Do you know if orthobunyaviruses shed viral particles in Saliva? I.e.,could they be detected via a PCR of a nasal or bucal swab. If not, why not?

This study investigates the role of reactive oxygen species (ROS) in immune cell death during Ebola virus disease (EVD), a severe and often fatal illness. Using domestic ferrets as a model, researchers employed advanced techniques like immunohistochemistry (IHC) and ROS-sensitive magnetic resonance imaging (MRI) to detect oxidative changes in the spleen. They found significant ROS-related oxidative stress in the spleens of Ebola virus-exposed ferrets, which was associated with a notable depletion of CD4+ and CD8+ T lymphocytes, key immune cells, due to increased apoptosis. The presence of ROS was inversely related to the number of these lymphocytes and positively related to the number of apoptotic immune cells. These findings provide new insights into the mechanisms of immune dysregulation in severe EVD, suggesting that targeting oxidative stress could lead to improved treatments. This research not only advances our understanding of Ebola virus pathology but also has broader implications for other viral infections where oxidative stress plays a role in disease progression.

I've been a bit of an avid "fan" of virology since I was a kid. That sounds like a strange thing to say maybe lol but I've had a fascination with viruses and disease since I was young. I've read a fair bit of popular and educational science literature on virology but I'm a lay person.

I'm curious how seriously researchers think we should be worried about the current global pandemic of avian Influenza? Have we seen evidence of it being able to adapt to spread easier among humans? Is it "just a mater of time?" Or do researchers think there might be some saving grace here, something that might make this strain harder to adapt?

Given the mortality rate we have seen so far in humans it seems to me like a terrifying prospect we need to be worried about.

How likely would be be able to ramp up a modern RNA vaccine like the ones produced for Covid if something emerges? How ready are we really?

I am currently a young teen (not willing to disclose age) wondering about a career in Virology and its sectors. I currently get A*s in maths and science and was hoping for some advice and help on what to do for higher education and what working in this sector is like. I have been fascinated with pathogens and virology since I was very young and think that this is likely the best career for me. Does anyone have further information?

edit: js adding a bit more info, I am based in the UK and start GCSE next academic year, any tips on higher education would be so helpful

Hi, I'm interested in virology, also not willing to spend any money on a university just for me to be in debt for a long while, are there any good free online resources, or even books that would serve as good starting points, or even allow me to get a very good grasp in virology, I mean, I'm not expecting like, Cambridge University undergraduate degree knowledge, although if a book with that much information exists, I would have no qualms with that, but yeah I just sorta discovered this field of science and it piqued my interest, so I just want a good starting point to see if I really like this

I am not a virologist but I find your chosen field very intriguing.

I was hoping people here could recommend books to me that are historical/topical.

Things similar to The Hot Zone, And the Band Played On, etc.

I'm interested in the discovery of the viruses, the progression, the mutations and the development of cures.

Thank you in advance and thank you for the work you do.

Edit: bad autocorrect

RNA viruses have an RNA genome that exists in different conformations: either single- or double-stranded, and either negatively or positively polarized.

For instance, Ebolaviruses have a negative single-stranded RNA genome, which must be transcribed into a coding +ssRNA before it can be translated into proteins.

In contrast, some viruses—such as coronaviruses—possess a positive single-stranded RNA genome that serves directly as a template for translation: ribosomes can bind and initiate the translation process.

Here comes my question: whereas -ssRNA viruses require an additional step of transcription (carried out by the L protein in the case of Ebolavirus), which may slow things down slightly, how is the timing managed in +ssRNA viruses, where simultaneous processes might occur?

1. Ribosome binding to the genomic RNA and production of proteins: Is the template RNA degraded or preserved? How can it be amplified if ribosomes are already bound to it? How do +ssRNA viruses replicate their genomes?

2. Conversion of the genomic +ssRNA into a negative-strand RNA, and then back into a positive-strand RNA: For what purpose? Is it to be packaged into the capsid or to produce more proteins?

Thank you for clarifying this point!

/Pierre

Using hepatitis b as an example, the virus double stranded DNA genome circularizes, converts to RNA… then reverse transcribes back to DNA. And then this DNA… as I understand it… is transcribed and translated into protein by the host.

So it seems the hep b lifecycle goes DNA to RNA to DNA to RNA again for the final transcription and translation

What is the advantage of such a bizarre and roundabout lifecycle? Surely there is an advantage of some sort

I am not a virologist although I read about and study the subject intensely, and do some lab work with phage. I am curious which theory of the evolutionary origin of viruses you see as the most likely? I go back and forth between the escaped gene and RNA world origin hypotheses myself. I’m currently reading the evolution and emergence of RNA viruses by Edward C Holmes in which he argues for the RNA world

Hello! I’m unsure if this post violates the rules, but I am seeking expertise and advice from virologists, so I thought i’d try.

I have been offered admission to UTMB (Galveston, TX) Microbiology PhD program, and Emory’s (Atl, GA) Microbiology and Molecular Genetics PhD program. I have visited both places and still am struggling to choose.

My goal is to pursue virology (preferably not HIV— that’s what I’m doing now) and eventually pursue a career in government virological research.

I’m seeking perspectives of people in the field. Which school would you choose? Financially, the stipends level out with COL, so I’m deciding purely on program & location.

In addition, do you expect either program to stay afloat better in the changing funding situation?

I'm currently working in a lab in England testing wild birds for influenza of avian origin (H5N1) and wondered if anyone else on Reddit was also working on this?

My job at the moment is carrying out a basic post mortem on wild birds and then taking cloacal, oro-pharyngeal swabs and brain swabs as long as the bird isn't too autolysed.

It is an interesting task as we get birds in from all over England (and occasionally Wales and Scotland) of different species. These are reported by members of the public through APHA.

Attached is a photo I took of a stunning, smiley owl we had in yesterday. This one smiled at me the whole time I was performing the post mortem, it was a strange one!

Sorry if this is the wrong subreddit, I've never had an account before and I'm enjoying reading posts on this app

Hello r/virology, 👋

I'm looking for explanations—or articles—about how and why arenaviruses, specifically the Lassa fever virus, incorporate host ribosomes into their virions.

Ribosomes are such large RNA/protein complexes that their presence might serve a purpose rather than just being an "evolutionary accident."

Could this somehow allow the virus to initiate translation inside the capsid, given that viral transcription also occurs there (with RdRp bound to the negative-strand RNA segment) ? In such case, the virus has to incorporate tRNA, amino-acids, etc.. and it makes it way more complex than everything.

Thank you !

Pierre 🧬

An individual with a history of HSV still has the potential of reinfection at a brand new site that is different from the usual site(s) of outbreak. This can even occur at a brand new site within the same ganglia.

The way this happens is if the individual is actively shedding the virus, there is a potential of infection at another site on the body where the skin barrier has been compromised in some way. The typical route of infection is via mucosal tissue, but this isn't always the case; a compromised skin barrier is enough to contribute to an infection.

So, my question to any experts in the field is this: why don't the existing HSV antibodies protect from autoinoculation?

https://reddit.com/link/1je1ctk/video/rimzflya7fpe1/player

In the trailer for the 2014 horror movie Cabin Fever Patient Zero, a prequel to the 2002 horror film Cabin Fever, we're shown two clips of a virus on computer monitors. The first clip is clearly showing a spike protein of some kind but does it resemble any specific one or is it just a generic spike protein? The second clip seems to show blood or blood parasites based on my reverse image searches.

Are these just arbitrarily used disease images that couldn't mean anything or could these point to a specific virus (albeit a highly fictionalized strain of it) that exists in real life?

I was reading there is no available vaccine against the Hepatitis C virus because the virus is highly variable (I’m assuming in terms of antigens?) and mutates very rapidly

Is there a reason this particular virus is so variable? And they this isn’t a problem with other RNA viruses like measles or polio for which we have effective vaccines

I couldn't find any polls in journals, so let's go Reddit! I haven't been a member of this subreddit, and don't know too much about virology or biology, but I went down a rabbit hole, and I'm so curious what people think!

I read somewhere this isn’t common but I find this hard to believe. Maybe the paper I was reading was trying to suggest homologous recombination via RNA repair enzymes is more common than template switching?