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What is the name of the property of viruses can activate a second time, with different symptoms?

What is the name of the property of viruses can activate a second time, with different symptoms?



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The Varicella zoster virus causes chickenpox in children and shingles in adults.

It appears after the initial infection, it can go dormant in the nerve, and reactivate itself decades later.

In chickenpox - the symptoms are:

characteristic skin rash that forms small, itchy blisters, which eventually scab over. It usually starts on the chest, back, and face then spreads to the rest of the body

In shingles - the symptoms are:

a painful skin rash with blisters involving a limited area. Typically the rash occurs on either the left or right of the body or face in a single stripe.

My question is: What is the name of the property of viruses can activate a second time, with different symptoms?


Viral latency is the best term to use for viruses that can lie dormant.

I have not come across a specific term for latent viruses that recur with different symptoms. This is probably because "different" is very subjective. Many pathogens can cause several different forms of disease depending on factors such as the route of exposure (i.e. where and how the pathogen got to its destination). Obviously the latent infection has a different pathophysiology to chickenpox. Due to its latency in dorsal root ganglia, shingles typically results in a localised rash, but there are less common disseminated forms of shingles that can look very similar to chickenpox.


What is the name of the property of viruses can activate a second time, with different symptoms? - Biology

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6.2 The Viral Life Cycle

All viruses depend on cells for reproduction and metabolic processes. By themselves, viruses do not encode for all of the enzymes necessary for viral replication. But within a host cell, a virus can commandeer cellular machinery to produce more viral particles. Bacteriophages replicate only in the cytoplasm, since prokaryotic cells do not have a nucleus or organelles. In eukaryotic cells, most DNA viruses can replicate inside the nucleus, with an exception observed in the large DNA viruses, such as the poxviruses, that can replicate in the cytoplasm. With a few exceptions, RNA viruses that infect animal cells replicate in the cytoplasm. An important exception that will be highlighted later is Influenza virus.

The Life Cycle of Viruses with Prokaryote Hosts

The life cycle of bacteriophages has been a good model for understanding how viruses affect the cells they infect, since similar processes have been observed for eukaryotic viruses, which can cause immediate death of the cell or establish a latent or chronic infection. Virulent phages typically lead to the death of the cell through cell lysis. Temperate phages , on the other hand, can become part of a host chromosome and are replicated with the cell genome until such time as they are induced to make newly assembled viruses, or progeny virus es.

The Lytic Cycle

During the lytic cycle of virulent phage, the bacteriophage takes over the cell, reproduces new phages, and destroys the cell. T-even phage is a good example of a well-characterized class of virulent phages. There are five stages in the bacteriophage lytic cycle (see Figure 6.7). Attachment is the first stage in the infection process in which the phage interacts with specific bacterial surface receptors (e.g., lipopolysaccharides and OmpC protein on host surfaces). Most phages have a narrow host range and may infect one species of bacteria or one strain within a species. This unique recognition can be exploited for targeted treatment of bacterial infection by phage therapy or for phage typing to identify unique bacterial subspecies or strains. The second stage of infection is entry or penetration . This occurs through contraction of the tail sheath, which acts like a hypodermic needle to inject the viral genome through the cell wall and membrane. The phage head and remaining components remain outside the bacteria.

The third stage of infection is biosynthesis of new viral components. After entering the host cell, the virus synthesizes virus-encoded endonucleases to degrade the bacterial chromosome. It then hijacks the host cell to replicate, transcribe, and translate the necessary viral components (capsomeres, sheath, base plates, tail fibers, and viral enzymes) for the assembly of new viruses. Polymerase genes are usually expressed early in the cycle, while capsid and tail proteins are expressed later. During the maturation phase, new virions are created. To liberate free phages, the bacterial cell wall is disrupted by phage proteins such as holin or lysozyme. The final stage is release. Mature viruses burst out of the host cell in a process called lysis and the progeny viruses are liberated into the environment to infect new cells.

The Lysogenic Cycle

In a lysogenic cycle , the phage genome also enters the cell through attachment and penetration. A prime example of a phage with this type of life cycle is the lambda phage. During the lysogenic cycle, instead of killing the host, the phage genome integrates into the bacterial chromosome and becomes part of the host. The integrated phage genome is called a prophage . A bacterial host with a prophage is called a lysogen . The process in which a bacterium is infected by a temperate phage is called lysogeny . It is typical of temperate phages to be latent or inactive within the cell. As the bacterium replicates its chromosome, it also replicates the phage’s DNA and passes it on to new daughter cells during reproduction. The presence of the phage may alter the phenotype of the bacterium, since it can bring in extra genes (e.g., toxin genes that can increase bacterial virulence). This change in the host phenotype is called lysogenic conversion or phage conversion . Some bacteria, such as Vibrio cholerae and Clostridium botulinum, are less virulent in the absence of the prophage. The phages infecting these bacteria carry the toxin genes in their genome and enhance the virulence of the host when the toxin genes are expressed. In the case of V. cholera, phage encoded toxin can cause severe diarrhea in C. botulinum, the toxin can cause paralysis. During lysogeny, the prophage will persist in the host chromosome until induction , which results in the excision of the viral genome from the host chromosome. After induction has occurred the temperate phage can proceed through a lytic cycle and then undergo lysogeny in a newly infected cell (see Figure 6.8).

Link to Learning

This video illustrates the stages of the lysogenic life cycle of a bacteriophage and the transition to a lytic phase.


Contents

The Russian zoologist Ilya Ilyich Mechnikov (1845–1916) first recognized that specialized cells were involved in defense against microbial infections. [16] In 1882, he studied motile (freely moving) cells in the larvae of starfishes, believing they were important to the animals' immune defenses. To test his idea, he inserted small thorns from a tangerine tree into the larvae. After a few hours he noticed that the motile cells had surrounded the thorns. [16] Mechnikov traveled to Vienna and shared his ideas with Carl Friedrich Claus who suggested the name "phagocyte" (from the Greek words phagein, meaning "to eat or devour", and kutos, meaning "hollow vessel" [1] ) for the cells that Mechnikov had observed. [17]

A year later, Mechnikov studied a fresh water crustacean called Daphnia, a tiny transparent animal that can be examined directly under a microscope. He discovered that fungal spores that attacked the animal were destroyed by phagocytes. He went on to extend his observations to the white blood cells of mammals and discovered that the bacterium Bacillus anthracis could be engulfed and killed by phagocytes, a process that he called phagocytosis. [18] Mechnikov proposed that phagocytes were a primary defense against invading organisms. [16]

In 1903, Almroth Wright discovered that phagocytosis was reinforced by specific antibodies that he called opsonins, from the Greek opson, "a dressing or relish". [19] Mechnikov was awarded (jointly with Paul Ehrlich) the 1908 Nobel Prize in Physiology or Medicine for his work on phagocytes and phagocytosis. [7]

Although the importance of these discoveries slowly gained acceptance during the early twentieth century, the intricate relationships between phagocytes and all the other components of the immune system were not known until the 1980s. [20]

Phagocytosis is the process of taking in particles such as bacteria, parasites, dead host cells, and cellular and foreign debris by a cell. [21] It involves a chain of molecular processes. [22] Phagocytosis occurs after the foreign body, a bacterial cell, for example, has bound to molecules called "receptors" that are on the surface of the phagocyte. The phagocyte then stretches itself around the bacterium and engulfs it. Phagocytosis of bacteria by human neutrophils takes on average nine minutes. [23] Once inside this phagocyte, the bacterium is trapped in a compartment called a phagosome. Within one minute the phagosome merges with either a lysosome or a granule to form a phagolysosome. The bacterium is then subjected to an overwhelming array of killing mechanisms [24] and is dead a few minutes later. [23] Dendritic cells and macrophages are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters they engulf huge quantities of material and frequently release some undigested back into the tissues. This debris serves as a signal to recruit more phagocytes from the blood. [25] Phagocytes have voracious appetites scientists have even fed macrophages with iron filings and then used a small magnet to separate them from other cells. [26]

A phagocyte has many types of receptors on its surface that are used to bind material. [2] They include opsonin receptors, scavenger receptors, and Toll-like receptors. Opsonin receptors increase the phagocytosis of bacteria that have been coated with immunoglobulin G (IgG) antibodies or with complement. "Complement" is the name given to a complex series of protein molecules found in the blood that destroy cells or mark them for destruction. [27] Scavenger receptors bind to a large range of molecules on the surface of bacterial cells, and Toll-like receptors—so called because of their similarity to well-studied receptors in fruit flies that are encoded by the Toll gene—bind to more specific molecules. Binding to Toll-like receptors increases phagocytosis and causes the phagocyte to release a group of hormones that cause inflammation. [2]

The killing of microbes is a critical function of phagocytes that is performed either within the phagocyte (intracellular killing) or outside of the phagocyte (extracellular killing). [28]

Oxygen-dependent intracellular Edit

When a phagocyte ingests bacteria (or any material), its oxygen consumption increases. The increase in oxygen consumption, called a respiratory burst, produces reactive oxygen-containing molecules that are anti-microbial. [29] The oxygen compounds are toxic to both the invader and the cell itself, so they are kept in compartments inside the cell. This method of killing invading microbes by using the reactive oxygen-containing molecules is referred to as oxygen-dependent intracellular killing, of which there are two types. [14]

The first type is the oxygen-dependent production of a superoxide, [2] which is an oxygen-rich bacteria-killing substance. [30] The superoxide is converted to hydrogen peroxide and singlet oxygen by an enzyme called superoxide dismutase. Superoxides also react with the hydrogen peroxide to produce hydroxyl radicals, which assist in killing the invading microbe. [2]

The second type involves the use of the enzyme myeloperoxidase from neutrophil granules. [31] When granules fuse with a phagosome, myeloperoxidase is released into the phagolysosome, and this enzyme uses hydrogen peroxide and chlorine to create hypochlorite, a substance used in domestic bleach. Hypochlorite is extremely toxic to bacteria. [2] Myeloperoxidase contains a heme pigment, which accounts for the green color of secretions rich in neutrophils, such as pus and infected sputum. [32]

Oxygen-independent intracellular Edit

Phagocytes can also kill microbes by oxygen-independent methods, but these are not as effective as the oxygen-dependent ones. There are four main types. The first uses electrically charged proteins that damage the bacterium's membrane. The second type uses lysozymes these enzymes break down the bacterial cell wall. The third type uses lactoferrins, which are present in neutrophil granules and remove essential iron from bacteria. [33] The fourth type uses proteases and hydrolytic enzymes these enzymes are used to digest the proteins of destroyed bacteria. [34]

Extracellular Edit

Interferon-gamma—which was once called macrophage activating factor—stimulates macrophages to produce nitric oxide. The source of interferon-gamma can be CD4 + T cells, CD8 + T cells, natural killer cells, B cells, natural killer T cells, monocytes, macrophages, or dendritic cells. [35] Nitric oxide is then released from the macrophage and, because of its toxicity, kills microbes near the macrophage. [2] Activated macrophages produce and secrete tumor necrosis factor. This cytokine—a class of signaling molecule [36] —kills cancer cells and cells infected by viruses, and helps to activate the other cells of the immune system. [37]

In some diseases, e.g., the rare chronic granulomatous disease, the efficiency of phagocytes is impaired, and recurrent bacterial infections are a problem. [38] In this disease there is an abnormality affecting different elements of oxygen-dependent killing. Other rare congenital abnormalities, such as Chédiak–Higashi syndrome, are also associated with defective killing of ingested microbes. [39]

Viruses Edit

Viruses can reproduce only inside cells, and they gain entry by using many of the receptors involved in immunity. Once inside the cell, viruses use the cell's biological machinery to their own advantage, forcing the cell to make hundreds of identical copies of themselves. Although phagocytes and other components of the innate immune system can, to a limited extent, control viruses, once a virus is inside a cell the adaptive immune responses, particularly the lymphocytes, are more important for defense. [40] At the sites of viral infections, lymphocytes often vastly outnumber all the other cells of the immune system this is common in viral meningitis. [41] Virus-infected cells that have been killed by lymphocytes are cleared from the body by phagocytes. [42]

In an animal, cells are constantly dying. A balance between cell division and cell death keeps the number of cells relatively constant in adults. [12] There are two different ways a cell can die: by necrosis or by apoptosis. In contrast to necrosis, which often results from disease or trauma, apoptosis—or programmed cell death—is a normal healthy function of cells. The body has to rid itself of millions of dead or dying cells every day, and phagocytes play a crucial role in this process. [43]

Dying cells that undergo the final stages of apoptosis [44] display molecules, such as phosphatidylserine, on their cell surface to attract phagocytes. [45] Phosphatidylserine is normally found on the cytosolic surface of the plasma membrane, but is redistributed during apoptosis to the extracellular surface by a protein known as scramblase. [46] [47] These molecules mark the cell for phagocytosis by cells that possess the appropriate receptors, such as macrophages. [48] The removal of dying cells by phagocytes occurs in an orderly manner without eliciting an inflammatory response and is an important function of phagocytes. [49]

Phagocytes are usually not bound to any particular organ but move through the body interacting with the other phagocytic and non-phagocytic cells of the immune system. They can communicate with other cells by producing chemicals called cytokines, which recruit other phagocytes to the site of infections or stimulate dormant lymphocytes. [50] Phagocytes form part of the innate immune system, which animals, including humans, are born with. Innate immunity is very effective but non-specific in that it does not discriminate between different sorts of invaders. On the other hand, the adaptive immune system of jawed vertebrates—the basis of acquired immunity—is highly specialized and can protect against almost any type of invader. [51] The adaptive immune system is not dependent on phagocytes but lymphocytes, which produce protective proteins called antibodies, which tag invaders for destruction and prevent viruses from infecting cells. [52] Phagocytes, in particular dendritic cells and macrophages, stimulate lymphocytes to produce antibodies by an important process called antigen presentation. [53]

Antigen presentation Edit

Antigen presentation is a process in which some phagocytes move parts of engulfed materials back to the surface of their cells and "present" them to other cells of the immune system. [54] There are two "professional" antigen-presenting cells: macrophages and dendritic cells. [55] After engulfment, foreign proteins (the antigens) are broken down into peptides inside dendritic cells and macrophages. These peptides are then bound to the cell's major histocompatibility complex (MHC) glycoproteins, which carry the peptides back to the phagocyte's surface where they can be "presented" to lymphocytes. [15] Mature macrophages do not travel far from the site of infection, but dendritic cells can reach the body's lymph nodes, where there are millions of lymphocytes. [56] This enhances immunity because the lymphocytes respond to the antigens presented by the dendritic cells just as they would at the site of the original infection. [57] But dendritic cells can also destroy or pacify lymphocytes if they recognize components of the host body this is necessary to prevent autoimmune reactions. This process is called tolerance. [58]

Immunological tolerance Edit

Dendritic cells also promote immunological tolerance, [59] which stops the body from attacking itself. The first type of tolerance is central tolerance, that occurs in the thymus. T cells that bind (via their T cell receptor) to self antigen (presented by dendritic cells on MHC molecules) too strongly are induced to die. The second type of immunological tolerance is peripheral tolerance. Some self reactive T cells escape the thymus for a number of reasons, mainly due to the lack of expression of some self antigens in the thymus. Another type of T cell T regulatory cells can down regulate self reactive T cells in the periphery. [60] When immunological tolerance fails, autoimmune diseases can follow. [61]

Phagocytes of humans and other jawed vertebrates are divided into "professional" and "non-professional" groups based on the efficiency with which they participate in phagocytosis. [9] The professional phagocytes are the monocytes, macrophages, neutrophils, tissue dendritic cells and mast cells. [10] One litre of human blood contains about six billion phagocytes. [5]

Activation Edit

All phagocytes, and especially macrophages, exist in degrees of readiness. Macrophages are usually relatively dormant in the tissues and proliferate slowly. In this semi-resting state, they clear away dead host cells and other non-infectious debris and rarely take part in antigen presentation. But, during an infection, they receive chemical signals—usually interferon gamma—which increases their production of MHC II molecules and which prepares them for presenting antigens. In this state, macrophages are good antigen presenters and killers. However, if they receive a signal directly from an invader, they become "hyperactivated", stop proliferating, and concentrate on killing. Their size and rate of phagocytosis increases—some become large enough to engulf invading protozoa. [62]

In the blood, neutrophils are inactive but are swept along at high speed. When they receive signals from macrophages at the sites of inflammation, they slow down and leave the blood. In the tissues, they are activated by cytokines and arrive at the battle scene ready to kill. [63]

Migration Edit

When an infection occurs, a chemical "SOS" signal is given off to attract phagocytes to the site. [64] These chemical signals may include proteins from invading bacteria, clotting system peptides, complement products, and cytokines that have been given off by macrophages located in the tissue near the infection site. [2] Another group of chemical attractants are cytokines that recruit neutrophils and monocytes from the blood. [13]

To reach the site of infection, phagocytes leave the bloodstream and enter the affected tissues. Signals from the infection cause the endothelial cells that line the blood vessels to make a protein called selectin, which neutrophils stick to on passing by. Other signals called vasodilators loosen the junctions connecting endothelial cells, allowing the phagocytes to pass through the wall. Chemotaxis is the process by which phagocytes follow the cytokine "scent" to the infected spot. [2] Neutrophils travel across epithelial cell-lined organs to sites of infection, and although this is an important component of fighting infection, the migration itself can result in disease-like symptoms. [65] During an infection, millions of neutrophils are recruited from the blood, but they die after a few days. [66]

Monocytes Edit

Monocytes develop in the bone marrow and reach maturity in the blood. Mature monocytes have large, smooth, lobed nuclei and abundant cytoplasm that contains granules. Monocytes ingest foreign or dangerous substances and present antigens to other cells of the immune system. Monocytes form two groups: a circulating group and a marginal group that remain in other tissues (approximately 70% are in the marginal group). Most monocytes leave the blood stream after 20–40 hours to travel to tissues and organs and in doing so transform into macrophages [67] or dendritic cells depending on the signals they receive. [68] There are about 500 million monocytes in one litre of human blood. [5]

Macrophages Edit

Mature macrophages do not travel far but stand guard over those areas of the body that are exposed to the outside world. There they act as garbage collectors, antigen presenting cells, or ferocious killers, depending on the signals they receive. [69] They derive from monocytes, granulocyte stem cells, or the cell division of pre-existing macrophages. [70] Human macrophages are about 21 micrometers in diameter. [71]

This type of phagocyte does not have granules but contains many lysosomes. Macrophages are found throughout the body in almost all tissues and organs (e.g., microglial cells in the brain and alveolar macrophages in the lungs), where they silently lie in wait. A macrophage's location can determine its size and appearance. Macrophages cause inflammation through the production of interleukin-1, interleukin-6, and TNF-alpha. [72] Macrophages are usually only found in tissue and are rarely seen in blood circulation. The life-span of tissue macrophages has been estimated to range from four to fifteen days. [73]

Macrophages can be activated to perform functions that a resting monocyte cannot. [72] T helper cells (also known as effector T cells or Th cells), a sub-group of lymphocytes, are responsible for the activation of macrophages. Th1 cells activate macrophages by signaling with IFN-gamma and displaying the protein CD40 ligand. [74] Other signals include TNF-alpha and lipopolysaccharides from bacteria. [72] Th1 cells can recruit other phagocytes to the site of the infection in several ways. They secrete cytokines that act on the bone marrow to stimulate the production of monocytes and neutrophils, and they secrete some of the cytokines that are responsible for the migration of monocytes and neutrophils out of the bloodstream. [75] Th1 cells come from the differentiation of CD4 + T cells once they have responded to antigen in the secondary lymphoid tissues. [72] Activated macrophages play a potent role in tumor destruction by producing TNF-alpha, IFN-gamma, nitric oxide, reactive oxygen compounds, cationic proteins, and hydrolytic enzymes. [72]

Neutrophils Edit

Neutrophils are normally found in the bloodstream and are the most abundant type of phagocyte, constituting 50% to 60% of the total circulating white blood cells. [76] One litre of human blood contains about five billion neutrophils, [5] which are about 10 micrometers in diameter [77] and live for only about five days. [37] Once they have received the appropriate signals, it takes them about thirty minutes to leave the blood and reach the site of an infection. [78] They are ferocious eaters and rapidly engulf invaders coated with antibodies and complement, and damaged cells or cellular debris. Neutrophils do not return to the blood they turn into pus cells and die. [78] Mature neutrophils are smaller than monocytes and have a segmented nucleus with several sections each section is connected by chromatin filaments—neutrophils can have 2–5 segments. Neutrophils do not normally exit the bone marrow until maturity but during an infection neutrophil precursors called metamyelocytes, myelocytes and promyelocytes are released. [79]

The intra-cellular granules of the human neutrophil have long been recognized for their protein-destroying and bactericidal properties. [80] Neutrophils can secrete products that stimulate monocytes and macrophages. Neutrophil secretions increase phagocytosis and the formation of reactive oxygen compounds involved in intracellular killing. [81] Secretions from the primary granules of neutrophils stimulate the phagocytosis of IgG-antibody-coated bacteria. [82]

Dendritic cells Edit

Dendritic cells are specialized antigen-presenting cells that have long outgrowths called dendrites, [83] that help to engulf microbes and other invaders. [84] [85] Dendritic cells are present in the tissues that are in contact with the external environment, mainly the skin, the inner lining of the nose, the lungs, the stomach, and the intestines. [86] Once activated, they mature and migrate to the lymphoid tissues where they interact with T cells and B cells to initiate and orchestrate the adaptive immune response. [87] Mature dendritic cells activate T helper cells and cytotoxic T cells. [88] The activated helper T cells interact with macrophages and B cells to activate them in turn. In addition, dendritic cells can influence the type of immune response produced when they travel to the lymphoid areas where T cells are held they can activate T cells, which then differentiate into cytotoxic T cells or helper T cells. [84]

Mast cells Edit

Mast cells have Toll-like receptors and interact with dendritic cells, B cells, and T cells to help mediate adaptive immune functions. [89] Mast cells express MHC class II molecules and can participate in antigen presentation however, the mast cell's role in antigen presentation is not very well understood. [90] Mast cells can consume and kill gram-negative bacteria (e.g., salmonella), and process their antigens. [91] They specialize in processing the fimbrial proteins on the surface of bacteria, which are involved in adhesion to tissues. [92] [93] In addition to these functions, mast cells produce cytokines that induce an inflammatory response. [94] This is a vital part of the destruction of microbes because the cytokines attract more phagocytes to the site of infection. [91] [95]

Professional Phagocytes [96]
Main location Variety of phenotypes
Blood neutrophils, monocytes
Bone marrow macrophages, monocytes, sinusoidal cells, lining cells
Bone tissue osteoclasts
Gut and intestinal Peyer's patches macrophages
Connective tissue histiocytes, macrophages, monocytes, dendritic cells
Liver Kupffer cells, monocytes
Lung self-replicating macrophages, monocytes, mast cells, dendritic cells
Lymphoid tissue free and fixed macrophages and monocytes, dendritic cells
Nervous tissue microglial cells (CD4 + )
Spleen free and fixed macrophages, monocytes, sinusoidal cells
Thymus free and fixed macrophages and monocytes
Skin resident Langerhans cells, other dendritic cells, conventional macrophages, mast cells

Dying cells and foreign organisms are consumed by cells other than the "professional" phagocytes. [97] These cells include epithelial cells, endothelial cells, fibroblasts, and mesenchymal cells. They are called non-professional phagocytes, to emphasize that, in contrast to professional phagocytes, phagocytosis is not their principal function. [98] Fibroblasts, for example, which can phagocytose collagen in the process of remolding scars, will also make some attempt to ingest foreign particles. [99]

Non-professional phagocytes are more limited than professional phagocytes in the type of particles they can take up. This is due to their lack of efficient phagocytic receptors, in particular opsonins—which are antibodies and complement attached to invaders by the immune system. [11] Additionally, most nonprofessional phagocytes do not produce reactive oxygen-containing molecules in response to phagocytosis. [100]

Non-professional Phagocytes [96]
Main location Variety of phenotypes
Blood, lymph and lymph nodes Lymphocytes
Blood, lymph and lymph nodes NK and LGL cells (large granular lymphocytes)
Blood Eosinophils and Basophils [101]
Skin Epithelial cells
Blood vessels Endothelial cells
Connective tissue Fibroblasts

A pathogen is only successful in infecting an organism if it can get past its defenses. Pathogenic bacteria and protozoa have developed a variety of methods to resist attacks by phagocytes, and many actually survive and replicate within phagocytic cells. [102] [103]

Avoiding contact Edit

There are several ways bacteria avoid contact with phagocytes. First, they can grow in sites that phagocytes are not capable of traveling to (e.g., the surface of unbroken skin). Second, bacteria can suppress the inflammatory response without this response to infection phagocytes cannot respond adequately. Third, some species of bacteria can inhibit the ability of phagocytes to travel to the site of infection by interfering with chemotaxis. [102] Fourth, some bacteria can avoid contact with phagocytes by tricking the immune system into "thinking" that the bacteria are "self". Treponema pallidum—the bacterium that causes syphilis—hides from phagocytes by coating its surface with fibronectin, [104] which is produced naturally by the body and plays a crucial role in wound healing. [105]

Avoiding engulfment Edit

Bacteria often produce capsules made of proteins or sugars that coat their cells and interfere with phagocytosis. [102] Some examples are the K5 capsule and O75 O antigen found on the surface of Escherichia coli, [106] and the exopolysaccharide capsules of Staphylococcus epidermidis. [107] Streptococcus pneumoniae produces several types of capsule that provide different levels of protection, [108] and group A streptococci produce proteins such as M protein and fimbrial proteins to block engulfment. Some proteins hinder opsonin-related ingestion Staphylococcus aureus produces Protein A to block antibody receptors, which decreases the effectiveness of opsonins. [109] Enteropathogenic species of the genus Yersinia bind with the use of the virulence factor YopH to receptors of phagocytes from which they influence the cells capability to exert phagocytosis. [110]

Survival inside the phagocyte Edit

Bacteria have developed ways to survive inside phagocytes, where they continue to evade the immune system. [111] To get safely inside the phagocyte they express proteins called invasins. When inside the cell they remain in the cytoplasm and avoid toxic chemicals contained in the phagolysosomes. [112] Some bacteria prevent the fusion of a phagosome and lysosome, to form the phagolysosome. [102] Other pathogens, such as Leishmania, create a highly modified vacuole inside the phagocyte, which helps them persist and replicate. [113] Some bacteria are capable of living inside of the phagolysosome. Staphylococcus aureus, for example, produces the enzymes catalase and superoxide dismutase, which break down chemicals—such as hydrogen peroxide—produced by phagocytes to kill bacteria. [114] Bacteria may escape from the phagosome before the formation of the phagolysosome: Listeria monocytogenes can make a hole in the phagosome wall using enzymes called listeriolysin O and phospholipase C. [115]

Killing Edit

Bacteria have developed several ways of killing phagocytes. [109] These include cytolysins, which form pores in the phagocyte's cell membranes, streptolysins and leukocidins, which cause neutrophils' granules to rupture and release toxic substances, [116] [117] and exotoxins that reduce the supply of a phagocyte's ATP, needed for phagocytosis. After a bacterium is ingested, it may kill the phagocyte by releasing toxins that travel through the phagosome or phagolysosome membrane to target other parts of the cell. [102]

Disruption of cell signaling Edit

Some survival strategies often involve disrupting cytokines and other methods of cell signaling to prevent the phagocyte's responding to invasion. [118] The protozoan parasites Toxoplasma gondii, Trypanosoma cruzi, and Leishmania infect macrophages, and each has a unique way of taming them. [118] Some species of Leishmania alter the infected macrophage's signalling, repress the production of cytokines and microbicidal molecules—nitric oxide and reactive oxygen species—and compromise antigen presentation. [119]

Macrophages and neutrophils, in particular, play a central role in the inflammatory process by releasing proteins and small-molecule inflammatory mediators that control infection but can damage host tissue. In general, phagocytes aim to destroy pathogens by engulfing them and subjecting them to a battery of toxic chemicals inside a phagolysosome. If a phagocyte fails to engulf its target, these toxic agents can be released into the environment (an action referred to as "frustrated phagocytosis"). As these agents are also toxic to host cells, they can cause extensive damage to healthy cells and tissues. [120]

When neutrophils release their granule contents in the kidney, the contents of the granule (reactive oxygen compounds and proteases) degrade the extracellular matrix of host cells and can cause damage to glomerular cells, affecting their ability to filter blood and causing changes in shape. In addition, phospholipase products (e.g., leukotrienes) intensify the damage. This release of substances promotes chemotaxis of more neutrophils to the site of infection, and glomerular cells can be damaged further by the adhesion molecules during the migration of neutrophils. The injury done to the glomerular cells can cause kidney failure. [121]

Neutrophils also play a key role in the development of most forms of acute lung injury. [122] Here, activated neutrophils release the contents of their toxic granules into the lung environment. [123] Experiments have shown that a reduction in the number of neutrophils lessens the effects of acute lung injury, [124] but treatment by inhibiting neutrophils is not clinically realistic, as it would leave the host vulnerable to infection. [123] In the liver, damage by neutrophils can contribute to dysfunction and injury in response to the release of endotoxins produced by bacteria, sepsis, trauma, alcoholic hepatitis, ischemia, and hypovolemic shock resulting from acute hemorrhage. [125]

Chemicals released by macrophages can also damage host tissue. TNF-α is an important chemical that is released by macrophages that causes the blood in small vessels to clot to prevent an infection from spreading. [126] However, if a bacterial infection spreads to the blood, TNF-α is released into vital organs, which can cause vasodilation and a decrease in plasma volume these in turn can be followed by septic shock. During septic shock, TNF-α release causes a blockage of the small vessels that supply blood to the vital organs, and the organs may fail. Septic shock can lead to death. [13]

Phagocytosis is common and probably appeared early in evolution, [127] evolving first in unicellular eukaryotes. [128] Amoebae are unicellular protists that separated from the tree leading to metazoa shortly after the divergence of plants, and they share many specific functions with mammalian phagocytic cells. [128] Dictyostelium discoideum, for example, is an amoeba that lives in the soil and feeds on bacteria. Like animal phagocytes, it engulfs bacteria by phagocytosis mainly through Toll-like receptors, and it has other biological functions in common with macrophages. [129] Dictyostelium discoideum is social it aggregates when starved to form a migrating pseudoplasmodium or slug. This multicellular organism eventually will produce a fruiting body with spores that are resistant to environmental dangers. Before the formation of fruiting bodies, the cells will migrate as a slug-like organism for several days. During this time, exposure to toxins or bacterial pathogens has the potential to compromise survival of the species by limiting spore production. Some of the amoebae engulf bacteria and absorb toxins while circulating within the slug, and these amoebae eventually die. They are genetically identical to the other amoebae in the slug their self-sacrifice to protect the other amoebae from bacteria is similar to the self-sacrifice of phagocytes seen in the immune system of higher vertebrates. This ancient immune function in social amoebae suggests an evolutionarily conserved cellular foraging mechanism that might have been adapted to defense functions well before the diversification of amoebae into higher forms. [130] Phagocytes occur throughout the animal kingdom, [3] from marine sponges to insects and lower and higher vertebrates. [131] [132] The ability of amoebae to distinguish between self and non-self is a pivotal one, and is the root of the immune system of many species of amoeba. [8]


Viral Infection

Viruses are present in almost every ecosystem on earth. They are marked as the most abundant biological entity on this planet. But sometimes these largely present entities cause trouble in human body. Viral Infection is one of the most common ailments affecting people. In simple parlance, a disease that is/can be caused by different types of virus is known as Viral Infection. It can affect various parts of the human body. It is observed that some viruses are in the intestine, while many are in lungs and airways. When infected, a patient may complain about abdominal pain, diarrhea, coughing and breathlessness.

Viruses can be spread or transmitted through various ways. Some people may get a viral infection by swallowing or inhaling virus, by being bitten by insects, through sexual contact or through transfusion of contaminated blood.

How does Viral Infection affect human body?

Viruses can be termed hijackers, as they invade healthy, living and normal cells to produce and multiply other viruses like them. These small infectious organisms need a living cell for reproduction. Hence they enter the host cell and release their DNA or RNA inside the host cell. This DNA or RNA contains the information which is required to replicate the virus. The interesting thing about viruses is that they are extremely unique microorganisms since they cannot reproduce without a host cell. So, after entering the host cell, the genetic material of the virus takes charge of the host cell and compels it to replicate the virus. In this operation, usually, the infected cell dies as the virus stops it from performing its usual functions. The entire process makes the human body feel weak and sick. Basically, a viral infection is a common term for many kinds of diseases caused by a virus. What do these diseases have in common, except for the virus? It is the symptoms like high fever, fatigue and body pain that makes the patient feel miserable.

There are many kinds of viruses- gastro intestinal viruses and airways viruses, being the most common ones. These viruses mostly cause fatigue and fever. Other viruses cause other local symptoms such as laryngitis, shingles and cold sores.

What are the different types of Viral Infections?

The most common type of virus led infection is the Respiratory Infection.

Respiratory infection affects the throat, upper airways and lungs. Most common respiratory infection includes a sore throat, common cold, sinus, pneumonia and influenza. Respiratory infection causes a lot of troubles in infants, older people and people suffering from lung or heart disorder.

Apart from respiratory infection, these can affect other specific parts/organs of the human body:

  • Liver: The presence of virus in liver can result in Hepatitis
  • Gastrointestinal tract: The existence of virus in the gastrointestinal tract, like gastroenteritis, is usually caused by rotavirus and norovirus.
  • Nervous System: Certain viruses like rabies virus and west nile virus infect human brain and cause encephalitis. There are some other viruses as well that infect the tissue layer covering the brain and spinal cord. These can cause meningitis.
  • Skin: There are some kind of viruses that cause skin infection which result in blemishes or warts. Many viruses that affect other body organs/parts, like chickenpox can cause rashes on the skin.

What diseases are caused by viruses?

Many human diseases are caused by virus led infections. These include:

  • Smallpox
  • Cold
  • Chickenpox
  • Measles
  • Hepatitis
  • Human Papiloma Virus
  • Influenza
  • Shingles
  • Herpes
  • Polio
  • Rabies
  • HIV (Human Immunodeficiency Virus)
  • Cold Sores
  • Ebola
  • SARS (Severe Acute Respiratory Syndrome)
  • Epstein-Barr Virus
  • Dengue
  • Some types of Cancer

What are the common symptoms of Viral Infection?

  • High Fever
  • Tiredness or Fatigue
  • Headache
  • Diarrhea
  • Sore throat
  • Abdominal Pain
  • Coughing
  • Runny nose
  • Skin rash
  • Nausea and vomiting
  • Muscle ache
  • Chills
  • Stiffness in neck
  • Seizures
  • Loss of sensation
  • Impaired bladder
  • Impaired bowel function
  • Paralysis of limbs
  • Sleepiness
  • Confusion

It is important to note here that not all the people who show these signs or symptoms need medical treatment. If the symptoms are mild, it is advised to wait for a few days as most of them disappear on their own. This is basically due to the activation of body’s own defense mechanism that destroys the virus and make the symptoms to fade away.

When is a Viral Infection serious?

Almost every person has had a flu or a bad cold at least once in their lifetime. So usually, a viral infection is not that serious. However, at times, such infections can become extremely troublesome. Below mentioned are some of the scenarios when a virus led infection can be considered serious:

  • Complaints and symptoms lasting for more than seven days
  • High fever lasting for more than five days
  • Breathlessness
  • New reddish rash or spots on the body

Body’s defense against Viral Infection

When a human body detects a viral infection, it begins to respond accordingly. A process commonly known as RNA interference starts which degrade viral genetic material, thereby enabling cells to outlast the infection.

Human body has several defense mechanisms against such infections. Skin is a primary physical barrier which discourages easy access to virus. Infected body cells make substances known as interferons that can make uninfected cells impervious to viral infection.

When the virus enters a human body, it triggers body’s immune defense mechanism. This defense mechanism starts with white blood cells (WBC), like monocytes and lymphocytes, which comprehend to attack and destroy the virus or the infected cell. If the body manages to survive the infection, the white blood cells remember the invader virus and can react more quickly and smartly to a further infection caused by the same virus. This response mechanism is called immunity.

Body’s immune system produces specific antibodies which are capable of binding to the viruses, thereby making them non-infectious. Apart from this, T-cells are sent to demolish the virus.

Though most of the viral infections produce a protective response from body’s immune system, viruses like Human Immunodeficiency Virus (HIV) specialize in damaging the immune system through different techniques.

What to do when infected with Viral Infection?

When it comes to an infection caused by a virus, the treatment is a little difficult as viruses live inside the body’s cells. They are ‘protected’ or ‘immunized ’ from most of the medicines. There are few basic things that a patient suffering from such infection should keep in mind:

  • Take adequate rest
  • Keep yourself well hydrated
  • Eat light food
  • Wash your hands regularly to avoid infection spreading to others

Unlike bacterial infections which can be treated with medicines/antibiotics, viral infections require either vaccinations to prevent them spreading at the first stage or antiviral drug to treat them. Vaccinations are usually the cheapest way to prevent virus led infections. It is also one of the most effective ways to counter such infections. Vaccinations are available for polio, mumps, rubella, measles among others. It is important to mention that vaccination has played a huge and instrumental role in eliminating diseases like smallpox, and reducing many other viral diseases to an extremely rare status.

Another interesting thing to note is that infections cause by virus tend to resolve on their own, without any treatment. Till the time infection is present in the body, the treatment mostly focuses on providing relief to the symptoms one is experiencing such as fever, cold/cough, pain etc.

Viral Infection in Children

Viral infection is common amid children as compared to adults. This is because, the immune system of a child is not as strong as that of a grown up and hence, the infection persists for a longer duration in their body. Sometimes virus infections become very serious while some just make a child feel unwell. Many a times, children develop fever, headache, runny nose, fatigue. These signs are a result of the battle between the virus and the body’s immune system. Hence, it is important to take care of certain things when a child is infected with virus led infection:

  • It is imperative that small babies and children should rest when they are affected with viral infection.
  • Since young children cannot blow their nose, parents can use rubber suction bulb to suck drainage from both sides of the child’s nose.
  • Children should be given sufficient lukewarm water and fruit juices, soups to keep them well hydrated.
  • Parents must avoid giving milk to infants as it can result in congestion.
  • Parents should also use hot steam to loosen the mucus in child’s nasal passage and chest.

If the viral infection persists for more than five days, the child should be taken to a doctor.

More on Viral Infection

It is noteworthy that many viruses that were present in very few parts of the world once are now spreading all over. These viruses include Chikungunya Virus, Zika Virus, Japanese Encephalitis Virus, West Nile Virus, Rift Valley Fever Virus etc. one of the main reasons of these viral infections spreading across is the changing climate that has resulted in more breeding areas for the mosquitoes that spread the deadly viruses. Another reason could be travelers getting infected from a virus, then returning home after being bitten by the mosquito that spread virus to others. Chikungunya is a typical example of this. Chikungunya is spread though mosquitoes and was first identified in Africa but has now spread to Caribbean and Central, South and North America. In Chikungunya viral infection, the patient experiences high fever, headache, muscle and joint pain, swelling and / or body rash.


Potential Achilles' heel of SARS-CoV-2 virus captured on video

Credit: Pixabay/CC0 Public Domain

Proteins known as lectins can bind to the spike protein on the SARS-CoV-2 virus and prevent it from accessing human cells, an international team of researchers led by the University of British Columbia's Dr. Josef Penninger has demonstrated.

They have captured the action on the pathogen's spike protein via video.

"Lectins are proteins that can bind the sugar molecule structure on lipids or proteins such as the spike protein," explains Dr. Penninger, director of the Life Sciences Institute in Vancouver. "Our idea is to harness this property to develop a drug to combat COVID-19 disease."

The researchers developed the largest lectin library in the world to find two lectins that are particularly adept at binding to glycans on the SARS-CoV-2 spike protein.

The approach is based on the idea behind the drug candidate APN01, currently in advanced clinical trials. APN01 is designed to lock out ACE2 receptors on cellular surfaces, and prevent SARS-CoV-2's spike from reaching the target it uses to infect and replicate.

"We are working with lectins on the same principle," said Penninger. "But the lectins would occupy neuralgic sites directly on the spike protein and thus disrupt the pathogen's binding to the cells. The door is blocked because the key is gummed up with lectins."

The S-protein, as the spike is known, is the structure that SARS-CoV-2 uses—with surprising agility—to grasp its target on cells and infect them. S-proteins cloak themselves in glycans to hide themselves from the host's immune system while they latch onto cells in the bloodstream, and major organs.

"We have now tools at hand that can bind the virus's protective layer and thereby block the virus from entering cells," says Dr. Stefan Mereiter, one of the first authors of the manuscript. "Moreover, these glycan-sites are highly conserved among all circulating SARS-CoV-2 variants, so this could be its Achilles' heel."

Collaborator Dr. Peter Hinterdorfer and his colleagues at the Institute for Biophysics at the University of Linz measured which binding forces and how many bonds occur between the lectins and the S-protein.

"We also filmed this bond," added Dr. Hinterdorfer. The scientists attached the spike protein that had been isolated at the University of Natural Resources and Life Sciences (Boku), Vienna, to a surface in a solution, and recorded the processes on film. "What is spectacular about the video is that you can see the dynamics of the spike protein."

The mobility captured by this method surprised the researchers, as the three-sided S-protein always looks relatively closed in still microscopy photographs.

"We saw that it actually opens up on the surfaces, and that the three arms are dynamic," said Dr. Hinterdorfer. "The lectins, on the other hand, were able to attach themselves to the structure for a long time on a biological scale."

Attachment times of up to around one second are actually a long service life for a molecular connection.


How people get infected with anthrax

People get infected with anthrax when spores get into the body. When anthrax spores get inside the body, they can be &ldquoactivated.&rdquo When they become active, the bacteria can multiply, spread out in the body, produce toxins (poisons), and cause severe illness.

This can happen when people breathe in spores, eat food or drink water that is contaminated with spores, or get spores in a cut or scrape in the skin. It is very uncommon for people in the United States to get infected with anthrax.

Certain activities can also increase a person&rsquos chances of getting infected.


JC Virus, Multiple Sclerosis, and Crohn's Disease

PML has been linked to the drug natalizumab (Tysabri), used to treat MS and Crohn's disease. People with MS or Crohn's disease may be tested for the JC virus before they start this medication or others like it. If you're a carrier of the virus, you might still be able to take the drugs, but discuss the risks and benefits with your doctor.

People with MS and Crohn's disease who develop PML often have to stop taking the drugs. They also may have a procedure called plasma exchange to clear out the medication.


Helper virus

any member of a unique class of infectious agents, which were originally distinguished by their smallness (hence, they were described as &ldquofiltrable&rdquo because of their ability to pass through fine ceramic filters that blocked all cells, including bacteria) and their inability to replicate outside of and without assistance of a living host cell. Because these properties are shared by certain bacteria ( rickettsiae, chlamydiae ), viruses are now characterized by their simple organization and their unique mode of replication. A virus consists of genetic material, which may be either DNA or RNA, and is surrounded by a protein coat and, in some viruses, by a membranous envelope.

Unlike cellular organisms, viruses do not contain all the biochemical mechanisms for their own replication they replicate by using the biochemical mechanisms of a host cell to synthesize and assemble their separate components. (Some do contain or produce essential enzymes when there is no cellular enzyme that will serve.) When a complete virus particle ( virion ) comes in contact with a host cell, only the viral nucleic acid and, in some viruses, a few enzymes are injected into the host cell.

Within the host cell the genetic material of a DNA virus is replicated and transcribed into messenger RNA by host cell enzymes, and proteins coded for by viral genes are synthesized by host cell ribosomes. These are the proteins that form the capsid (protein coat) there may also be a few enzymes or regulatory proteins involved in assembling the capsid around newly synthesized viral nucleic acid, in controlling the biochemical mechanisms of the host cell, and in lysing the host cell when new virions have been assembled. Some of these may already have been present within the initial virus, and others may be coded for by the viral genome for production within the host cell.

Because host cells do not have the ability to replicate &ldquoviral RNA&rdquo but are able to transcribe messenger RNA, RNA viruses must contain enzymes to produce genetic material for new virions. For certain viruses the RNA is replicated by a viral enzyme ( transcriptase ) contained in the virion, or produced by the host cell using the viral RNA as a messenger. In other viruses a reverse transcriptase contained in the virion transcribes the genetic message on the viral RNA into DNA, which is then replicated by the host cell. Reverse transcriptase is actually a combination of two enzymes: a polymerase that assembles the new DNA copy and an RNase that degrades the source RNA.

In viruses that have membranes, membrane-bound viral proteins are synthesized by the host cell and move, like host cell membrane proteins, to the cell surface. When these proteins assemble to form the capsid, part of the host cell membrane is pinched off to form the envelope of the virion.

Some viruses have only a few genes coding for capsid proteins. Other more complex ones may have a few hundred genes. But no virus has the thousands of genes required by even the simplest cells. Although in general viruses &ldquosteal&rdquo their lipid envelope from the host cell, virtually all of them produce &ldquoenvelope proteins&rdquo that penetrate the envelope and serve as receptors. Some envelope proteins facilitate viral entry into the cell, and others have directly pathogenic effects.

Some viruses do not produce rapid lysis of host cells, but rather remain latent for long periods in the host before the appearance of clinical symptoms. This carrier state can take any of several different forms. The term latency is used to denote the interval from infection to clinical manifestations. In the lentiviruses , it was formerly mistakenly believed that virus was inactive during this period. The true situation is that lentiviruses are rapidly replicating and spawning dozens of quasi-species until a particularly effective one overruns the ability of the host's immune system to defeat it. Other viruses, however, such as the herpesviruses , actually enter a time known as &ldquoviral latency,&rdquo when little or no replication is taking place until further replication is initiated by a specific trigger. For many years all forms of latency were thought to be identical, but now it has been discovered that there are different types with basic and important distinctions.

In viral latency, most of the host cells may be protected from infection by immune mechanisms involving antibodies to the viral particles or interferon . Cell-mediated immunity is essential, especially in dealing with infected host cells. Cytotoxic lymphocytes may also act as antigen-presenting cells to better coordinate the immune response . Containment of virus in mucosal tissues is far more complex, involving follicular dendritic cells and Langerhans cells .

Some enveloped RNA viruses can be produced in infected cells that continue growing and dividing without being killed. This probably involves some sort of intracellular regulation of viral growth. It is also possible for the DNA of some viruses to be incorporated into the host cell DNA, producing a carrier state. These are almost always retroviruses , which are called proviruses before and after integration of viral DNA into the host genome.

Few viruses produce toxins, although viral infections of bacteria can cause previously innocuous bacteria to become much more pathogenic and toxic. Other viral proteins, such as some of the human immunodeficiency virus , appear to be actively toxic, but those are the exception, not the rule.

However, viruses are highly antigenic. Mechanisms of pathologic injury to cells include cell lysis induction of cell proliferation (as in certain warts and molluscum contagiosum ) formation of giant cells, syncytia, or intracellular inclusion bodies caused by the virus and perhaps most importantly, symptoms caused by the host's immune response , such as inflammation or the deposition of antigen-antibody complexes in tissues.

Because viral reproduction is almost completely carried out by host cell mechanisms, there are few points in the process where stopping viral reproduction will not also kill host cells. For this reason there are no chemotherapeutic agents for most viral diseases. acyclovir is an antiviral that requires viral proteins to become active. Some viral infections can be prevented by vaccination (active immunization ), and others can be treated by passive immunization with immune globulin , although this has been shown to be effective against only a few dozen viruses.


Prevention of HPV

The first HPV vaccine came on the market in 2006, and within six years of its introduction, infections with HPV types 6, 11, 16, and 18 had decreased by 64 percent among teen girls ages 14 to 19, and by 34 percent among women ages 20 to 24, according to an article published in February 2016 in the journal Pediatrics. (7)

HPV types 6 and 11 cause 90 percent of genital warts, and types 16 and 18 cause most cases of HPV-related cancer.

A subsequent systematic review and meta-analysis published in June 2019 in The Lancet confirmed the impact of HPV vaccination. (8) The meta-analysis included data on 60 million people from 14 different countries that had set up HPV vaccine programs in the previous 10 years.

Public Health Officials Push for More Effort Vaccinating Kids Against HPV

It showed that HPV infections dropped by 83 percent among girls ages 13 to 19 and 66 percent among women aged 20 to 24. For genital warts, the drop was 67 percent among teen girls ages 15 to 19, 54 percent for women ages 20 to 24, and 31 percent for those ages 25 to 29. Precancerous cervical lesions also dropped, by 51 percent among teens ages 15 to 19 and 31 percent among women ages 20 to 24.

The study also showed that genital warts among males dropped 48 percent for those ages 15 to 19 and 32 percent for those ages 20 to 24. The researchers attributed the lower rates among teen boys and men to herd protection provided by the vaccination of young women.

At least two studies have also found that HPV vaccination lower rates of oropharyngeal HPV infections. One, published in January 2018 in the Journal of Clinical Oncology, studied young adults ages 18 to 33 in the United States from 2011 to 2014. (9) A second, published in June 2020 in The Journal of Infectious Diseases, studied men who have sex with men and transgender women age 18 to 26 in three U.S. cities during 2016 to 2018. (10)

The HPV vaccine currently used in the United States, Gardasil 9, protects against HPV types 6, 11, 16, and 18, as well as against five other types that can cause cancer: 31, 33, 45, 52, and 58.

Australian researchers have found that the HPV vaccine not only protects against genital warts and cancer, but also against childhood recurrent respiratory papillomatosis (RRP), an uncommon but incurable disease in which the virus causes wart-like growths to develop in the respiratory tract, eventually making it difficult to breathe. RRP is caused by HPV types 6 and 11, noted a study published in November 2017 in The Journal of Infectious Diseases. (11)

RRP that occurs in childhood is believed to be passed from mother to child around the time of birth. RRP can also occur in adults, usually in early adulthood, around the time HPV is commonly acquired through sexual transmission.

In the United States, the HPV vaccine is approved for preteens and adults through age 45. The CDC recommends that all adolescents get two doses of vaccine at age 11 or 12. (12)

For most people who get a first dose before their 15th birthday, only one more dose is needed, 6 to 12 months later. People who get their first dose on or after their 15th birthday need three doses total, with the second dose given one to two months after the first, and the third dose given six months after the first.

In spite of the proven protections offered by the HPV vaccine, not all Americans who could enjoy those benefits are getting them. Data released by the CDC on August 23, 2019, showed that during 2017 through 2018, coverage with one or more doses of HPV vaccine among teens ages 13 to 17 rose from about 66 percent to just over 68 percent, and the percentage of teens who had received all recommended doses of the HPV vaccine increased from about 49 percent to just over 51 percent, with the increases observed only among males. (13)

In contrast, in Australia in 2017, just over 80 percent of 15-year-old girls, and nearly 76 percent of 15-year-old boys had received three doses of the HPV vaccine, according to Cancer Australia. (14)


Watch the video: Properties: Commutative, Associative, Distributive, and Identity (August 2022).