virology blog

Not a book, but prof. Vincent Racaniello offers free courses[1] and has great youtube videos. [1]https://www.virology.ws/course/

Wouldn't the system somehow need to detect the virus at incredibly low PPM, and rely on the virus being in that section of the room? Especially with coronavirus, which travels via water droplets and falls to the ground fairly quickly, you could have a spreader walk through the room without it hitting the device. I'd also expect that the list of viruses that are worth evacuation over is much much shorter than the sum of all viruses in the air at one time. (Looked it up, looks like 219 viruses that can even just infect us[1] vs hundreds of millions [2]) [1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427559/ [2] https://www.virology.ws/2013/09/06/how-many-viruses-on-earth/

The author is Vincent Racaniello Ph.D., Professor of Microbiology & Immunology in the College of Physicians and Surgeons of Columbia University(https://www.virology.ws/about/) I absolutely recommend his virology lectures https://youtu.be/lj3NhPgOoX4

Question of mutation invariably comes up. I recommend this article: http://www.virology.ws/2020/01/23/a-lesson-from-sars-cov-for-2019-ncov… Summary: We know of deletion event in SARS Orf8, and amino acid change in ebola glycoprotein. In both cases, it decreased viral replication or virulence.

1200 mutations away from RATG-13 is how significant exactly? I will propose that it is not particularly significant. One virus I work with, I have 14 variants ranging from 300 to 500 base-pair differences. That is from passing in a laboratory only. I have one variant that has a 14000 BP deletion! (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217056/#mmi144... TABLE S2) However, it is noteworthy for that reason. That said, these are dsDNA viruses with comparatively much slower mutation rates. 1200-base differences are almost nothing. You're comparing apples and oranges. 14 mutational sites across a virus with 17k ssDNA genome is not comparable to RATG-13 vs SARS-2, which have not just 1200 mutations different, they're spread out over HUNDREDS of SNPs. That's the important comparator. And why it will take so long to mutate one into the other by natural mutation rates. >The two non-canonical arginines don't make it less likely? Not particularly. CGG exists in MERS 15 times. NL63, 29 times. It even exists twice in a row in Human coronavirus 229E. Throughout all of the known alphacoronaviruses (94 described) CGG exists 1575 times. In betacoronaviruses, it exists more times than my processor can count without hanging, and I believe it tops out at 9,999 events. I just ran blastn to figure that out. Using these datasets: https://www.ncbi.nlm.nih.gov/datasets/coronavirus/genomes/ Why is it so unlikely that synonymous mutational drift over the course of 70 years of infections…

Great overview of the biotech behind these COVID-19 nanobodies by Vincent Racaniello [1]: > Human monoclonal antibodies that block infection with SARS-CoV-2 are being used to treat COVID-19 patients, but an alternative, antibodies produced in camelids (alpacas and llamas) might have advantages. Camelid monoclonal antibodies can be more cheaply produced in mass quantities in bacteria, and protein engineering can be quickly used to produce a better therapeutic product. Nanobodies are small and stable enough to be delivered as a nasal spray unlike the current mabs (Regeneron and Eli Lilly) that are delivered intravenously. The paper An ultrapotent synthetic nanobody neutralizes SARS-CoV-2 by stabilizing inactive Spike [2] was discussed in the podcast TWiV 708: Alpaca llama full of nanobodies [3] on Jan 7th. Unfortunately this spray is too late to impact the course of the current pandemic but it gives hope for the future. [1] https://www.virology.ws/2021/01/14/camelids-for-covid/ [2] https://science.sciencemag.org/content/370/6523/1473 [3] https://www.microbe.tv/twiv/twiv-708/

I'm sorry to hear about your wife, that sounds awful. I also had post COVID issues, I couldn't get out of bed for a month and was very low energy for three. The doctors did nothing for me but luckily I have now recovered on my own. I tried eating lots of vegetables and lean meat (as per official nutritional recommendations) and it made me worse. I remember building up the strength every day just to chop the vegetables, eat and go back to bed. When I told my Doctor they dismissed it. I recovered on a diet of fatty red meat (1-2lb per day), milk, cream, eggs and fruit. The diet could be a timing coincidence but on the other hand maybe my Grandmother was on to something feeding me beef stew when I was ill as a kid. There will be a law suit over how CFS patients are currently treated: https://www.virology.ws/2020/07/15/trial-by-error-nice-on-exercise-and… You might want to follow it. I will be.

I have chronic fatigue syndrome since a bad viral infection in 2001. I find this article quite unfortunate. There is plenty of good research being done into CFS that does not generate the outrage that the PACE trial has. There are many reasons that particular study has been the focus of campaigners while other researchers are encouraged or left in peace, but I would encourage those who are coming to this issue here for the first time to do some more reading before coming to an opinion. The abstract to the study itself is here (the full study is behind Elsevier paywall): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065633/?report=reader David Tuller's blog critiquing the study is at: http://virology.ws Searching for "PACE trial" will bring up plenty of articles on either side of the debate. My own thought as to why this particular study stirred so much controversy is that it has been seized on by some in the medical-political establishment in the UK as defining a solution for all CFS sufferers, and negating the need for further study into the condition (although recent hearings in UK Parliament have begun to reverse this approach), when really the effect demonstrated by the study is quite small. Fortunately, the US establishment has not taken this tack: http://nationalacademies.org/hmd/Reports/2015/ME-CFS.aspx https://www.cdc.gov/me-cfs/index.html CFS remains a poorly-understood disease with a grossly underfunded research program when the number of people affected…

...if you want to learn about the true beauty of viruses, learn about how they work, how their genetic code is written and "executed" to produce the simplest and smallest possible viable replicator (though not an independent replicator), grab a molecular virology textbook like [1] (it's not that hard - you can skim a more general molec bio book like [2], which is written in a style very friendly to all technically oriented people, including coders). Or check out a really cool virology blog - http://www.virology.ws/ (by one of the authors of book [1]), though latest posts are more about politics and social implications than cool basic science. I have a feeling that von Newman would be extremely fascinated by modern molecular virology if he'd be alive today, considering his interest for minimal universal replicators [3]. If you think about it, modern computer science may very well owe its existence to von Newman's and Turing's interest in mathematical models of life itself! (...if you want to learn more about the topic above, just google "von newman universal constructor" or "turing morphogenesis" or "schrodinger what is life" and start exploring, I don't want to spoil anyone's fun of finding out about this for yourselves :) ) --- [1] http://astore.amazon.com/virologyws-20/detail/1555814433 [2] http://www.amazon.com/Molecular-Biology-Cell-Bruce-Alberts/dp/08153410… [3]…

We haven't found any mitoviruses in animals, yet, at least? 1: https://virology.ws/2019/03/28/viruses-that-infect-mitochondria/

Some microbiologists think they are alive: https://www.nature.com/articles/454677a Others don't think so: https://virology.ws/2020/12/03/pandoraviruses-are-not-alive/

Very very very low. Bacteria and viruses are normally very sensitive to their hosts, they have a kind of symbiosis that means they can't just arbitrarily infect any species they bump into. Jumping between species does happen, and when it happens it can be a big problem (see COVID-19, Swine Flu), but there is something like 100 million different virus species out there [1], and only 200 or so are able to infect humans [2]. Despite constant interaction between people and all other species of viral host all over the globe, and millions of brand new new virus exposures daily, jumps are still so rare that they are decade-defining when they happen. 1. https://virology.ws/2013/09/06/how-many-viruses-on-earth/ 2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427559/

> viruses have the most stripped down genomes of all Giant viruses can have over 1M basepairs, substantially larger than a bacteria such as Mycoplasma genitalium, with substantial functionality (pretty much everything except the ribosome in at least some of them: https://www.virology.ws/2018/03/08/only-the-ribosome-is-lacking/)

To add to this, how many virions are needed for a successful replication to start depends on the virus. https://www.virology.ws/2011/01/21/are-all-virus-particles-infectious/

He covered accident lab release in Question 4 [0]. He mentions that the WIV lab is well respected, well funded, well equipped, there was public logging of all relevant bat samples, along with parallel samples sent to other labs, lab workers were not the first who were sick, and there's genetic evidence that the virus did not originate in Wuhan. Dr. Duehr links to a reference that talks about the cleavage site [1], which concluded that "Acquisition of the furin cleavage site might be viewed as a ‘gain of function’ that enabled a bat CoV to jump into humans and begin its current epidemic spread" [0] https://old.reddit.com/r/science/comments/gk6y95/covid19_did_not_come_… [1] https://www.virology.ws/2020/02/13/furin-cleavage-site-in-the-sars-cov…

... or eating the flesh of any animal Edit: ... or eating plants: https://www.virology.ws/2015/06/25/prions-in-plants/

I didn't downvote you (can't even if I wanted to since you replied to me!), but the difference in outcomes is unlikely to be explained solely by differing strains, and there's no evidence at this time that the mutations have any biologically meaningful difference: https://www.virology.ws/2020/05/07/there-is-one-and-only-one-strain-of…

Reinfection can occur with most viruses when a person is exposed too soon after the primary immune response. It takes a while for someone to develop full immunity after recovery. This happened with H1N1 for patients back in 2008. https://www.virology.ws/2009/12/28/reinfection-with-2009-influenza-h1n…

This is not correct. https://www.virology.ws/2017/02/17/viral-rna-is-not-infectious-virus/

Also, wear a set of goggles at all times. Please prevent the particles from being contracted in your eyes. http://www.virology.ws/2018/03/01/influenza-virus-in-the-eye/

They have a recent blog post “A lesson from SARS-CoV for 2019-nCoV”: http://www.virology.ws/2020/01/23/a-lesson-from-sars-cov-for-2019-ncov…

I don't think it's the most likely explanation, far from it, but it wouldn't have to be a bioweapon to have been released from a lab. The reemergence of H1N1 in 1977 is believed to have been the result of a lab accident or vaccine trial gone awry, for example: http://www.virology.ws/2009/03/02/origin-of-current-influenza-h1n1-vir…

Valacyclovir http://www.virology.ws/2018/11/08/herpes-simplex-virus-and-alzheimers-…

> Also, vaccines can run horribly off the rails. One cannot mutate into a pathogen, as you say The live polio vaccine absolutely can. Before polio was largely eliminated, it didn't really matter, but once the risk of getting the wild-type virus dropped below the risk of getting it from the vaccine, it stopped making sense to use the live-attenuated vaccine. http://www.virology.ws/2015/09/10/why-do-we-still-use-sabin-poliovirus…

You're right, I appreciate the correction. For any one curious, here's more detail on the resistance that has been developed: http://www.virology.ws/2015/06/12/resistance-to-prion-disease-in-human…

The information around Alzheimers seems to be heading the direction that the beta-amyloid plaques are an immune response to the HSV1 herpes virus that help prevent the spread of the virus.[1] I suppose it can't be ruled out yet that this immune response could still cause damage, but it does make me wonder if the plaques are actually responsible at all for the symptoms seen, since like you said, other drugs reduce the plaques with no improvement in symptoms. It's interesting that this treatment seems to work when others do not- when they seem to be accomplishing the same thing (reduction of beta-amyloid plaques) [1] http://www.virology.ws/2018/11/08/herpes-simplex-virus-and-alzheimers-…

This is exactly the wrong interpretation. We know that cannibalism causes prion disease, and we have known that for as long as we have known about prion disease. the question is not whether cannibalism causes prion disease, which it definitely does, but whether past cannibalism was common enough to have selected for some innate resistance to it. http://www.virology.ws/2015/06/12/resistance-to-prion-disease-in-human…

http://www.virology.ws/2009/06/02/pathogenesis-of-influenza-in-humans/ To keep your coworkers from getting the flu, go home as soon as you think you might be coming down with something. The amount of virus you are shedding into your environment is nicely exponential in how bad you are feeling, with one exception: The day before you start feeling really bad, you are shedding nearly as much virus as when you are feeling worst. If you have to choose, it's better to go home early and come back before you are feeling 100%, than it is to stay at work until you are certain you are sick and stay home longer. It's always better to shift your sick days earlier in the illness.

I've been taking magnesium supplements for the past few months. Coincidentally, I've been blowing my nose continually for the past week. Wasn't aware there could be a potential link. Edit: Although, I've been taking a Zinc supplement (as well as a D3 supplement) and according to my lay-understanding of this blog-post[a], the Zinc should cancel out magnesium's effect? [a] http://www.virology.ws/2009/12/16/rhinovirus-and-zinc-part-5-magnesium…

Oh yes it is: - 1924-1925 smallpox outbreak and mass vaccinations in Duluth, Minneapolis, and St. Paul: http://www.mnopedia.org/event/smallpox-epidemic-1924-1925 - 1947 smallpox outbreak and mass vaccinations in New York City: http://www.virology.ws/2009/12/22/smallpox-in-new-york-city-1947/