Question about enveloped RNA virus viral genome

Question about enveloped RNA virus viral genome

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I am a newbie studying campbell biology. just a quick question about virus. When viral genome(RNA) expose itself in the host cell, why does the host cell not eliminate the genome since it apparently not belong to the cell ? Is there any mechanism that the host cell can detect and eliminate the viral genome as in the step 2,3 in the figure below ?

Thanks in advance !

Your image illustrates the replication cycle of a negative-sense single-stranded RNA virus, where the viral genome needs to be "inverted" by an RNA polymerase into mRNA before being translated by the host. There are many examples of (-)ssRNA viruses, including filoviruses (Ebola, Marburg), paramyxoviruses (measles, mumps), orthomyxoviruses (influenza), rhabdoviruses (rabies), deltaviruses (Hepatitis D), and others.

These (and all) viruses evolved alongside their hosts, and consequently the hosts evolved various protection mechanisms. One primitive component of the so-called innate immune system in humans and other organisms (going back at least to plants) are proteins known as pattern recognition receptors (PRRs) which bind to conserved motifs found in microbes, including possible pathogens. The types of molecules recognized by these PRRs include certain types of carbohydrate moieties like LPS, peptidoglycans and other components of bacterial cell walls, fungal glucans, bacterial peptides, some types of microbial nucleic acids (such as single- and double-stranded RNA, more on this in a bit), chitin, and others.

One class of PRRs are the Toll-like receptors (TLRs), named after the Drosophila Toll protein. They recognize a wide variety of microbial patterns and activate downstream signaling to stimulate an immune response, including production of pro-inflammatory cytokines and anti-viral interferons. In our case, two of them are particularly important - TLR3 and TLR7. TLR3 recognizes double-stranded RNA, which occurs transiently during (-)ssRNA virus infection when the negative-sense genome is being copied to positive-sense mRNA. However, dsRNA is much more common in retroviral infections. TLR7 recognizes single-stranded RNA in endosomes, which would occur after macrophages, dendritic cells, or B cells consume dead virally-infected cells.

Unfortunately for the host cell, once it has been infected there isn't much that can be done to save it. Viruses evolved to hijack the cell's machinery and make more copies of themselves. This hijacking is generally one way, so the only way to fight the infection is to kill the cells producing the viruses. This is, for example, why you often get a sore throat during an influenza or rhinovirus (one of the most common causative agents of the common cold) infection - epithelial cells lining the throat get infected, and are killed by the immune system to prevent the spread of the infection. This leaves a "raw" area that must heal over time.

A common class of enveloped single-stranded RNA viruses are the Alphaviruses. They are typically spread through insect bites, usually mosquitoes. These viruses carry a single strand of "positive" RNA, which is 5' capped and has a 3' Poly Adenosine tail, making it appear like a normal mammalian messenger RNA, only much larger.

Because this RNA is positive, ribosomes in your cells can directly use this RNA to produce the enzymes needed to duplicate the RNA. These replicases use the positive strand to create many negative strands. Each negative strand can then be used to create additional copies of the positive strand as well many more copies of the subgenomic RNA, which is used to create the capsid and envelope proteins. Those proteins plus the positive strand RNAs are assembled into new viruses and bud off the cell.

The viral RNA protects itself by acting like a messenger RNA. This recruits host proteins that prevent degradation and promote translation to make the viral proteins. Most alphaviruses also shut down host-cell transcription and inhibit the interferon response. This prevents the cell from mounting a defense against infection, but also eventually kills the cell.

EDIT: I just noticed that your question is tagged "Retrovirus", but your image does not represent the retrovirus life-cycle. It looks more like an alphavirus life-cycle.

Depending on the nature of the viral genome there are multiple pathways (elaborated upon in previous answers and comments) that sense viral nucleic acids and trigger an interferon response. This can induce apoptosis and kill infected cells, or alternatively, it can set of a cascade of genes that induce replication arrest (which in the case of some viruses can be enough to thwart an infection because of viral dependence on host replication factors).

One byproduct of the induction of an interferon response is the induction of the APOBEC family of cytodine deaminases, which can hypermutate viral genomes (APOBEC1 hits RNA, multiple APOBEC3 proteins hit DNA/ssDNA that may potentially result from various phases of the replication cycle), and other related restriction factors.

However viruses have evolved to evade these responses, either by altering restriction factors themselves, or by evolving sequences that won't be detected by viral sensing molecules.

If you are trying to ask if the RNA can be destroyed, it is not likely unless you don't utilize siRNA.

SiRNA, a mechanism involved in the regulation of phenotype expression, plays a key role in avoiding lytic and lysogenic cycles that could potentially help the virus produce virions, helping the virus reproduce. This RNA, also known as small (short) interfering RNA, an RNA duplex, is able to target certain mRNA molecules, causing them to degrade. This can eventually lead to gene knockdown.

Additionally, the lysogenic cycle, causing cells to lay dormant for some time before eventually releasing virions, contains a g0 phase. The g0 phase is a period of the cell cycle in which the cell produces minimal proteins or undergoes little or no DNA replication. Keeping the cell in this phase may help avoid virion synthesis.

Furthermore, being able to trigger immediate cell apoptosis would also help reduce the amount of viral replication. However, this can be dangerous as the cell may be prone to undergoing the lytic cycle.

So yes, it may be possible without the use of siRNA, but it will be very unlikely. Immune response can also help fight off the virions in the long run.

  • In a double stranded RNA form, retroviruses infect a host cell with their genome, and then are reverse transcribed into double stranded DNA, with the DNA then integrated into the home cell genome.
  • When integrated into a host genome, a retrovirus is hard to detect and can lay dormant for prolonged periods, having no discernible effect on the host.
  • Retroviruses can be human pathogens, and cause many diseases, but have also proven to be invaluable tools when used by molecular biologists.
  • reverse transcriptase: An enzyme that catalyzes the formation of DNA from RNA found in retroviruses.
  • transposon: A segment of DNA that can move to a different position within a genome.
  • integrase: Any enzyme that integrates viral DNA into that of an infected cell.

A retrovirus is an RNA virus that is duplicated in a host cell using the reverse transcriptase enzyme to produce DNA from its RNA genome. The DNA is then incorporated into the host&rsquos genome by an integrase enzyme. The virus thereafter replicates as part of the host cell&rsquos DNA. Retroviruses are enveloped viruses that belong to the viral family Retroviridae. A special variant of retroviruses are endogenous retroviruses, which are integrated into the genome of the host and inherited across generations. Endogenous retroviruses are a type of transposon.

The virus itself stores its nucleic acid in the form of an mRNA genome and serves as a means of delivering that genome into cells it targets as an obligate parasite (a parasite that cannot live without its host). That process of delivering the genome into cells constitutes the infection. Once in the host&rsquos cell, the RNA strands undergo reverse transcription in the cytoplasm and are integrated into the host&rsquos genome, at which point the retroviral DNA is referred to as a provirus. It is difficult to detect the virus until it has infected the host, where the provirus can stay for months, even years, before becoming active and making new infectious viral particles.

In most viruses, DNA is transcribed into RNA, and then RNA is translated into protein. Retroviruses, however, function differently. Their RNA is reverse-transcribed into DNA, which is integrated into the host cell&rsquos genome (when it becomes a provirus), and then undergoes the usual transcription and translation processes to express the genes carried by the virus. So, the information contained in a retroviral gene is used to generate the corresponding protein via the sequence: RNA &rarr DNA &rarr RNA &rarr protein. Retroviruses can be pathogens of many different hosts, including humans. A notable retrovirus is Human immunodeficiency virus (HIV), the virus responsible for acquired immunodeficiency syndrome (AIDS). As well as infecting a host, some retroviruses can cause cancer.

Figure: HIV viral life cycle: This diagram depicts the viral life cycle of HIV, from infection, integration into a host genome, reconstruction, and formation of new viral particles. The inset on the left depicts an individual HIV particle.

Finally, retroviruses are proving to be valuable research tools in molecular biology and have been successfully used in gene delivery systems.

The Complexities of +RNA Virus Cell Biology

Positive-strand viruses replicate in the cytoplasm of the host cell in association with cytoplasmic membranes. To complete a productive infection, they must enter cells, institute cytoplasmic replication factories, replicate genome RNA, express their genomes, sort and traffic proteins and RNA, and assemble and release virus particles—in some cases within an 8–12 hour life cycle. Investigators who seek to dissect the replication strategies of +RNA viruses are drawn inexorably into the complexities of cellular biology. To determine the mechanisms by which +RNA viruses navigate these steps may necessitate an understanding of cell biology processes as diverse as cytoplasmic organelle structure and membrane biogenesis, endoplasmic reticulum (ER) formation, microtubule motor movement, actin polymerization, and trafficking in the secretory pathway. +RNA viruses also share a common requirement for translation of the input mRNA-sense +RNA genome to yield nonstructural proteins that are responsible for both induction of membrane modifications and RNA replication and transcription. These genomes range in size and complexity from the small, segmented 4.5 kb flock house virus (FHV) genome to the 27–32 kb nonsegmented coronavirus (CoV) genomes, which express an

800 kDa replicase fusion polyprotein processed by multiple viral proteinases into 16 mature nonstructural proteins (nsp1 to 16) [1].

Linking Evolutionary Change at the Intrahost and Interhost Scales

Large population sizes, rapid replication, and extremely high mutation rates mean that populations of RNA viruses usually harbor extensive genetic diversity [8]. Despite this, the vast majority of studies of genetic diversity in RNA viruses, particularly for acute infections, have been conducted at the epidemiological level, in which a single consensus sequence is generated from each infected individual. This sequence must then describe the average diversity in the intrahost viral population, masking myriad variable mutant sequences, some of which may have a major bearing on fitness. However, determining the extent and structure of intrahost genetic variability and how it relates to that observed at the epidemiological scale is of fundamental importance for understanding many aspects of evolutionary dynamics, including the likelihood of successful cross-species transmission and emergence [9].

For studies of RNA virus evolution to truly come of age, it is critical that the relationship between intra- and interhost evolution be explored in depth. Major questions include: What is the fitness distribution of mutations sampled from within hosts? Do the processes of intra- and interhost differ in fundamental ways? What proportion of intrahost diversity is passed between hosts at transmission? Thankfully, the barriers of time and cost that prohibited studies of this kind in the past have now largely been dismantled in the age of genomics. Experimental infections may represent a particularly profitable research avenue in which intrahost evolution is documented in samples collected every few days (or even hours), and also allowing viruses to be passed among hosts, thereby providing a window on the dynamics of interhost transmission.

Question about enveloped RNA virus viral genome - Biology

The study of animal viruses contributes to our understanding of the molecular basis of viral infection in general. The emergence of the SARS virus in the human population, coming from an animal source, highlights the importance of animals in harbouring infectious agents. In addition it has been recognized recently that influenza viruses, which persist in their natural avian host, can directly infect humans.

In this book an international panel of leading virologists provide a state-of-the-art overview of the field, comprehensively detailing the current understanding of viruses, their replication, evolution and interaction with the host. The authors emphasize strategic and methodological aspects of current research, and provide key related references. Topics include foot-and-mouth disease virus, Pestivirus, Arteriviridae, Coronaviruses (including SARS), Herpesviridae, Paramyxoviridae, influenza viruses, Reoviridae, porcine circoviruses, Asfarviridae and much more.

An essential text for all virology laboratories.

". a thorough, up-to-date review of the molecular biology of a number of key animal viruses . " from Microbiology Today (2008)

800 Å) the atomic structure of proteins and the internal capsid (

700 Å, the first large highly complex structure ever solved) the definition of the virus encoded enzymes required for RNA replication the ordered assembly of the capsid shell and the protein sequestration required for it and the role of host proteins in virus entry and virus release. These areas are important for BTV replication but they also indicate the pathways that may be used by related viruses, which include viruses that are pathogenic to man and animals, thus providing the basis for developing strategies for intervention or prevention.

(EAN: 9781904455226 9781913652197 Subjects: [virology] [microbiology] [medical microbiology] [molecular microbiology] )

A High School Q&A About Covid–19

Picture of Broughton High students courtesy of Ms. Tara Stremic.

Students and teachers have as many questions about Covid-19 as anyone. Here we answer questions posed by Ms. Tara Stremic, a biology teacher at Broughton High School in Raleigh, North Carolina and her students. These are a mix of questions aimed at making sense of how Covid-19 impacts our (and their) daily lives and questions that help to fit the unfolding evolutionary story of the virus that causes Covid-19 into the unfolding (and now online) high school biology curriculum. Below, Dr. Matt Koci , a virologist at North Carolina State University answers Tara’s questions.

Ms. Stremic: How exactly did the SARS-CoV-2 virus jump from an animal host to humans in Wuhan (was it eaten, breathed in?)

Dr. Matt Koci: The short and honest answer is we don’t know for sure, but there is no evidence that the virus is being transmitted in food. All evidence is this is primarily being spread like the flu or other cold viruses, in coughs and sneezes. So I would assume the first jump was also by breathing it in. That assumption is based on what we think happened in the early 2000s with the first SARS-Coronavirus. Food handlers in live animal markets, who had more direct contact with the live animals were at higher risk of getting the disease than others, suggesting that eating infected food wasn’t a major means of transmission.

Ms. Stremic: What determines how a virus is transmitted from host to host? Is it just the outer viral proteins?

Dr. Matt Koci: I’m assuming you’re asking within a species, which is to say, “what determines how it moves from person-to-person?”

So in the case of coronavirus, what determines it would be spread by coughs and sneezes and not by mosquitos, right? Thinking of host-to-host in this case, the answer is typically a function of where in the body does it replicate and what’s the least complicated way it can get to that same tissue in a new host. So if you’re a virus that replicates in the lung, the easiest path to a new lung is to be coughed out and breathed into someone else. If you’re a virus-like norovirus that replicates in the intestine and causes diarrhea, your shortest distance to a new host is causing your host to poop all over the place in the hopes that someone swallows some of the resulting mess (life is gross) and you find your way into the intestine of someone new.

Now if by host-to-host you mean from one species to another, that’s a little different. Here yes, the outer proteins play a big part, but that’s just one step in the chain. The host cell receptor in the new host (species) needs to be similar enough to the cell receptor in the original species that the virus can bind to it, even if the binding isn’t perfect. If that condition is met, all the other steps associated with virus entry into the cell also need to be similar enough. If the virus requires other host proteins (secondary receptors or host enzymes) they also have to be present at the right concentration and conserved between host species so the virus can recognize and use those, too. Then, once the virus gets inside and uncoats and starts to replicate (see answer below about life cycle) all the other viral proteins used to take over the cell, they need to recognize these other host proteins, especially those whose job is focused on blocking innate immune defenses.

Ms Stremic: Does the shape/size/genome size of a virus correlate to its fatality/contagiousness?

Dr. Matt Koci : No. There are viruses of all different types, shapes, and sizes (physically and genomically). What makes one more contagious or deadly than another has to do with the proteins it makes and how those proteins interact with your cells. A good example of that is the common cold coronaviruses these aren’t deadly, but they are the same size and shape as SARS-Cov-2. There are viruses that are much smaller than coronavirus that are much deadlier (Ebola comes to mind) and there are others that are even bigger that can be worse, think smallpox (we eradicated that decades ago). In each family of viruses, there can be a lot of variability in how they behave and the diseases they cause (we talk about how SARS-Cov-2 compares in size to other common viruses on this blog).

Ms Stremic: What are the types of cells in the body that this particular virus affects and what steps does it go through to make more copies of itself?

Dr. Matt Koci: So this virus uses the host cellular receptor ACE2 (angiotensin-converting enzyme 2). ACE2 is expressed on a lot of cells, so it has the ability to bind to, and possibly infect lots of different cells of the body. It is still not clear how many different cells the coronavirus is replicating in. Clearly, cells of the respiratory tract are involved, but there is also some evidence that maybe intestinal cells are also infected, but it could be others. It’s also not clear if the replication in these other cells is tied to worse disease.

From de Wit, E. et al. (2016). SARS and MERS: recent insights into emerging coronaviruses. Nature Reviews Microbiology, 14(8), 523.

The way this virus typically works (and several other enveloped viruses) is when the virus binds it triggers the cell to pull it inside (internalization) through a process known as endocytosis. This gets the virus inside the cell, but it’s not really inside the cell yet. It’s trapped inside a vesicle. To start taking over the cell and replicating, it needs to get out of the vesicle and release its genes and proteins into the cytoplasm. To do this, the Spike protein needs to be cut into 2 parts. This is called enzymatic cleavage and is typically done by host enzymes. This allows for the spike protein to change shape in a way that allows for the lipids in the virus coat and vesicle to fuse. This membrane-membrane fusion event triggers what’s called “uncoating”. So this fusion event is critical, which means the ability of the viral receptor protein to be cut is a critical step in the virus life cycle and regulating what cells/tissues it can infect (tissue tropism). Several host enzymes have been suggested to play a role in this cleavage step furin, cathepsin L and TMPRSS2, all trypsin-like proteases. I should also note that there is some evidence that the membrane fusion step can occur without endocytosis, so that step may not be necessary, but the cleavage of the spike to allow for membrane fusion is still a key step.

After uncoating, the viral RNAs are released into the cytoplasm of the cell. In the case of coronavirus, the RNA genome is what’s called positive-sense RNA. That means the viral RNA looks like messenger RNA to the host cell and starts making proteins off the viral genome, and this is really the start of the infection. (As a side note, the genomes of other RNA viruses like influenza are negative-sense RNA viruses. Their RNA genome is the reverse complement of messenger RNA, so the cell doesn’t make protein off it right away. These viruses bring along their own polymerase capable of making new RNA strands of RNA templates. When these viruses first uncoat, the viral polymerase converts the negative since RNA genome into positive-sense RNA that the cell then sees as mRNA and the infection takes off).

Once the cell starts making the viral proteins they (viral proteins) start doing their specific jobs. Some proteins are focused on “hijacking” the cell, making sure the cell’s machinery is dedicated to making virus products and not host products that the virus doesn’t need. Other proteins are involved in blocking host cell defenses against viruses. While other proteins are dedicated to making as many copies of new daughter genomes as possible. Once the cell has been largely exhausted of resources, the process reverses itself. The virus stops making copies of itself and starts to assemble new viral particles. In coronaviruses, a protein known as N binds to the RNA genome to help protect it, and shuttle the RNA to the place in the cell where it will be packaged into a new virus. For enveloped viruses, the structural membrane proteins (S, M, and E) will be inserted in a host membrane, the RNA will then bud through that membrane so the “vesicle” that comes off is a newly packaged virus with RNA inside. This is then released from the cell to go off and infect new cells.

To look at this process another way check out this video . It is from a biotech company trying to sell their technology for how to treat/prevent flu infections, but a lot of the principles are the same for coronavirus. Just don’t worry with anything after 2min 25s:

Ms Stremic: What specific immune system cells are involved that respond to this virus?

Dr. Matt Koci: In short, all of them. What we don’t know is which ones are helpful. It’s thought that in some of the most severe cases, a lot of the lung damage is from an overly aggressive immune response, but what cells drive that response and which cells lead to less severe disease is not clear. It does appear that antibodies are protective, so B-cell responses are clearly involved and likely a good thing. Being a viral infection killer T-cells are going to play a role, as are helper T-cells in coordinating the response of the others, but the devil is in the details on this response and right now we just don’t know enough details.

Ms Stremic: Why are different people more immune to the virus than others? What makes some people asymptomatic?

Dr. Matt Koci: This is the billion-dollar question right now, and we don’t know why some people are asymptomatic and others require serious medical help. We don’t even know how many people are asymptomatic. Hopefully, we will start testing more people, not just for the virus, but to see if they have antibodies to the virus to show that they were infected but didn’t get sick. Once we identify enough of these people we’ll be able to start to figure out what’s different between these groups.

This is a subtle difference, but I don’t think the asymptomatic people are immune. As far as we know today, this virus is so new and so different, no one should have prior immunity. We’ll likely find that some people are genetically resistant like we found with HIV and other diseases. We know the primary receptor for HIV is CD4 on CD4 positive T-cells however, HIV also needs another protein, CCR5. We actually figured that out when we identified some people who seemed to be resistant to infection and found that they had mutations in their CCR5 gene, so it wasn’t expressed. There may be something like that involved here. Another explanation is the severity of the disease is related to how aggressively your immune system reacts to the infection. Because of other medical conditions, other lung infections you’ve had, or other factors we don’t understand, in some people the immune system overreacts and ends up causing more damage than the virus does. This was also true with the first SARS outbreak, as well as people who have contracted the H5N1 bird flu. However, what causes the overreaction in some and not others is largely unknown.

One last comment on this, if you’re interested in how different infectious diseases have shaped human evolution and how some of the genetic diseases of today may be the results of disease selection pressure in the past, this–Survival Of The Sickest–is a good book.

Ms. Stremic: How long have viruses been around and what is the first ever documented case of a virus infecting humans?

Dr. Matt Koci: Viruses have been around likely since there have been cells. In fact, there’s one theory that self-replicating RNA (not that different from an RNA virus) might actually have developed before cell-based life. We’ll never know for sure, but without a doubt, viruses were around before humans, and so as soon as humans arrived, there would have been viruses to infect them. There is a small but growing field of viral archeology where people look for evidence that viruses played a role in some of the major events in early human history. For example, several viruses have been implicated as being part of the 10 plagues in the book of Exodus in the Bible.

Ms. Stremic: If viruses are not living, how does hand washing “kill” viruses?

Dr. Matt Koci: I love this question. So virologists and biologists continually debate what is the meaning of life. You would think defining what life is would be easy but it turns out it’s like defining what smart is. The definition that I think most people still learn is something like it has the capacity to grow, metabolize, respond (to stimuli), adapt, and reproduce. Based on this definition viruses aren’t alive only because grow, metabolize, and respond don’t fit, but everything else fits. They don’t grow because they never change size. They assemble. You will hear people say the virus grows in the lung, or something like that, but what they really mean is it replicates there. And the viruses require a lot of energy, nucleic acids, proteins and lipids, but they can’t make any of that on their own so they can’t metabolize. And they don’t run away if you poke them with a stick, but they do evolve in response to stimuli so it depends on how you define “respond”. I should say there are other definitions for life that some people use that have fewer criteria and under that definition viruses might qualify as a form of life.

Given how much they can do with so few genes, I certainly think they should be considered alive–why else would you learn about them in biology class? However, the general consensus among scientists is that they technically aren’t alive, so I’ll get off my soapbox and get back to your question. You’ll hear people talk about “killing” viruses, but when virologist talk we refer to it as “inactivating” the virus. In virology, viruses are either active (or they could also be referred to as infectious) OR they inactive. But, these distinctions typically aren’t that critical, so when non-virologist say things like “live virus vaccine”, “handwashing kills viruses”, or even the “virus grows in the lung” most virologists don’t get worked up about it. We recognize that words like active, inactive, replicate, and propagate are science jargon and might cause more confusion for others, so as long as the underlying concept being communicated is correct, that’s the important part. In fact, most of us use these phrases ourselves from time to time, but if you do and another virologist hears you, you’ll get a sarcastic, “Are you saying viruses are alive?”

So one other point to make about handwashing. You hear a lot in the news about handwashing vs. using hand sanitizer, and which is better at “killing” the virus. In both cases it’s about contact time. You need enough sanitizer to completely cover your hands, and the alcohol in the sanitizer needs to not evaporate off too quickly. Any virus that isn’t “killed” by the sanitizer is still on your hands. When you use soap and water, it’s also about contact time, that’s why they tell you to scrub for at least 20 seconds. The soap works on the lipids in the virus, but the water helps flush stuff off your hands, and then when you follow up by drying your hands with a paper towel you’re hopefully removing any more left behind. That said, either method is magic. They have to be done properly, and the more you do it the safer you’ll be. For good tips see the CDC’s page on handwashing.

Ms. Stremic: If we’re developing a vaccine for Covid-19, why don’t we have a vaccine for the common cold?

Dr. Matt Koci: This is another good question. I’m not sure the exact reason for this, but I suspect it related to 2 factors. First, while there are several coronaviruses that commonly cause the common cold, there are roughly 200 viruses from all different types of virus families (not coronaviruses) that can cause the common cold (the cold is really a set of multiple diseases with similar systems). To make vaccines to all these would just be too expensive to prevent a disease that while unpleasant for a few days, isn’t really life-threatening. The other factor is for reasons we don’t understand, our immunity to the common cold coronaviruses doesn’t seem to last very long, 6-months to a year. It’s not sure if a vaccine would work any better. Given enough time and research, we could probably make one, but people have decided it’s probably not worth the effort, again for something that’s not that bad of a disease.

There is a real concern that might also be true for this coronavirus. It’s possible that a vaccine to SARS-Cov-2 will only protect you for a 6-12months, which means you’ll need to be revaccinated every year, or even multiple times a year to keep up immunity. However, in this case, this virus causes enough of a disease, and affects enough people, that a vaccine would still be worth the effort.

Ms. Stremic: Does increasing temperature denature the proteins on the surface of the virus to destroy its shape? (based on videos circulating the internet claiming hairdryers and saunas can destroy it)

Dr. Matt Koci: So yes heating viruses, hot enough, long enough, will denature their proteins in ways that inactivate them. How hot and how long varies with different viruses, and it depends on what the virus is in. If it’s in water, it tends to be more susceptible to heat than–say–if it’s in snot. The extra proteins in snot help protect it. In many ways that’s what your body is trying to do when you get a fever. It’s trying to heat the place up (your body) but the fever is also a dangerous part of the disease. While you can sit in a sauna that is 140F, the cells of your body can’t handle that temperature. That’s why you sweat so much in a sauna to keep your core temp down. When your core body temp gets above 105F you are in serious danger.

To inactive viruses by heat you typically have to heat it up to 140-150F for several minutes (some viruses need even higher temps for longer). So yes, heat can destroy the virus, but you have to literally cook yourself to do it, so you’re dead anyway. A virology teacher I had years ago loved to say “viruses are the easiest pathogen to get rid of. If you want to kill the virus, kill the host.” But that doesn’t provide the medical outcome most people are hoping for, so the hairdryer and sauna are not going to help. If you’re still alive, so is the virus.

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    Bigelow Laboratory for Ocean Sciences, East Boothbay, ME, USA

    Joaquín Martínez Martínez

    Department of Physiology, Genetics, and Microbiology, University of Alicante, Alicante, Spain

    Francisco Martinez-Hernandez & Manuel Martinez-Garcia

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    All authors researched data for the article, contributed to the discussion of the content and reviewed and edited the manuscript before submission. M.M.-G. and J.M.M. wrote the article.

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    Diagnostic Virology Laboratory (DVL)

    The USGS National Wildlife Health Center's Diagnostic Virology Laboratory (DVL) performs isolation and identification of common and novel viruses from diagnostic and research samples.

    Isolation procedures used are specific to the host animal and suspected pathogen. The DVL has expertise in recognizing morphological changes in cell culture and effects on embryonated avian eggs caused by viral infection. Some of the identification techniques used include PCR, RT-PCR, serum neutralization, serology, electron microscopy, and DNA sequencing. The DVL participates in the Select Agent Program and is a member of the USDA National Animal Health Laboratory Network (NAHLN).

    Virology Laboratory Capabilities

    Virus isolation and propagation:

    • Perform virus isolation in tissue culture
      • Utilize cell lines appropriate to host animal, including Muscovy duck embryo fibroblasts (MSDEF), Madin-Darby canine kidney (MDCK), African green monkey kidney (VERO), and zebra fish (ZF4) cells
      • Microscopically detect typical cytopathic effect in cell culture for known viruses and atypical cytopathic effect for possible novel viruses
      • Allantoic inoculation [example: avian influenza virus (AIV) and avian paramyxovirus (APMV)]
      • Chorioallantoic membrane (CAM) inoculation [example: avian pox virus]

      Inoculation of embryonating chicken eggs. (NWHC. Public domain.)

      Identification of virus isolates:

      • Prepare electron microscopy grids for viewing virus particles
      • Perform virus-neutralizing tests using constant-serum varying-virus (example: duck plague) and constant-virus varying-serum (example: APMV)
      • Determine structure of viral nucleic acid and presence of lipid coat
      • Perform ELISA testing (example: Influenza types A and B, canine parvovirus)
      • Conduct molecular testing including nucleic acid extraction, PCR, and sequencing (see molecular testing below)

      Diagnostic technician looks at virology samples under a microscope. (NWHC. Public domain.)

      Characterization of novel virus isolates:

      • Determine optimal cell culture necessary and number of virus particles present (TCID50)
      • Describe morphology by electron microscopy
      • Determine pathogenicity by mean death time and/or EID50 in embryonated chicken eggs
      • Characterize viral nucleic acid as RNA or DNA and as enveloped with lipid coat or non-enveloped

      Serologic tests (antibody detection):

      • Conduct microtiter neutralization and plaque reduction assays to determine serum antibody titers for a variety of pathogens including
        • Crane Herpesvirus (Inclusion Body Disease in Cranes – IBDC)
        • AMPV subtypes 1-9
        • Novel common eider orthomyxovirus (Wellfleet Bay Virus)
        • West Nile virus (WNV)
        • St. Louis encephalitis virus (SLEV) & Japanese encephalitis virus (JEV)
        • Avian adenovirus
        • Eastern equine encephalitis virus (EEEV) and others

        Nucleic acid extraction, screening, and sequencing:

        • Employ multiple procedures for RNA and DNA extraction on tissue, swab, and environmental samples
        • Conduct molecular screening (PCR) for known viruses, including: AIV, APMV-1, WNV, Ranavirus, Wellfleet Bay virus, Duck Viral Enteritis Virus, Buggy Creek virus, avian poxvirus, flavivirus
        • Perform viral subtyping and phylogenetic analysis by Sanger, Next-generation, and whole genome sequencing methods

        Virology Diagnostic Tests

        The following is a reference guide to commonly requested tests. It is not a full list of testing capabilities of the laboratories. Determination of which test will be run on any given submission will be based on case history, gross findings at necropsy, and the scientific judgment of the case pathologist.

        SARS-CoV-2 structure and replication characterized by in situ cryo-electron tomography

        Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the COVID19 pandemic, is a highly pathogenic β-coronavirus. As other coronaviruses, SARS-CoV-2 is enveloped, replicates in the cytoplasm and assembles at intracellular membranes. Here, we structurally characterize the viral replication compartment and report critical insights into the budding mechanism of the virus, and the structure of extracellular virions close to their native state by in situ cryo-electron tomography and subtomogram averaging. We directly visualized RNA filaments inside the double membrane vesicles, compartments associated with viral replication. The RNA filaments show a diameter consistent with double-stranded RNA and frequent branching likely representing RNA secondary structures. We found that assembled S trimers in lumenal cisternae do not alone induce membrane bending but laterally reorganize on the envelope during virion assembly. The viral ribonucleoprotein complexes (vRNPs) are accumulated at the curved membrane characteristic for budding sites suggesting that vRNP recruitment is enhanced by membrane curvature. Subtomogram averaging shows that vRNPs are distinct cylindrical assemblies. We propose that the genome is packaged around multiple separate vRNP complexes, thereby allowing incorporation of the unusually large coronavirus genome into the virion while maintaining high steric flexibility between the vRNPs.

        Watch the video: RNA enveloped viruses ortho and paramyxo (June 2022).