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Q: Dr. Krishna, can one or two viral particles cause an infection?

Krishna: That  depends.

The average number of viral particles needed to establish an infection is known as the infectious dose.

The minimum dose of virus particles that can initiate infection, termed the minimum infective dose (MID).

Presence of pre-existing antibodies has been shown to affect the infectious dose and to be protective against reinfection for many, but not all viruses. 

In experimental models of diseases, we have many types of inoculi. You can have, for example, a sub-lethal inoculum which means that that amount of viable microorganisms to be delivered in the host will be incapable of causing a lethal disease. A lethal inoculum will be an amount of viable microorganisms that will be capable of causing a lethal disease (e.g. killing the host). A sub-clinical inoculum will not even cause a perceptible disease in the host.

In a immuno-supressed/immunodeficient host, a sub-clinical inoculum could cause a lethal disease. In a immunocompetent host, depending on the type of microorganism, even a very large inoculum can go unnoticed (no clinical sign will emerge).

 A number of factors may influence viruses’ infectivity in experimentally infected human volunteers. These include host and pathogen factors as well as the experimental methodology (3). These include host factors such as age, health status, and previous exposure to the virus; pathogen factors such as virulence of the viral strain and passage in cell culture; and experimental factors such as the route of inoculation and the sensitivity of the assay used to determine the viral dose administered.

This differs from virus to virus. For instance, Noroviruses (Norovirus is a very contagious virus that causes vomiting and diarrhea) 
are highly infectious: as few as 10 virus particles are needed to cause infection, and the ID50 is 18 particles.

We don’t know what this is for covid-19 yet, but given how rapidly the disease is spreading, it is likely to be relatively low – in the region of a few hundred or a thousand particles.
Can exposure to a single virus particle lead to infection or disease? Until now, solid proof has been lacking. Experimental research with insect larvae at Wageningen University and Simon Fraser University in Canada has shown that one virus particle is theoretically enough to cause infection and subsequent disease (1,2).

Studies suggest that the nasal infectious dose of influenza virus A is several orders of magnitude higher than that of airborne infection (4).

Therefore,  the infectious dose range is anywhere from 1 virus, to hundreds of millions. 

Q: What is a viral load?

Krishna: Viral load relates to the number of viral particles being carried by an infected individual and shed into their environment.

Usually the symptoms depend on the viral load the person carries.
If you have a high viral load, you are more likely to infect other people, because you may be shedding more virus particles. However, in the case of covid-19, it doesn’t necessarily follow that a higher viral load will lead to more severe symptoms (5,6).

If the infectious dose doesn’t correlate with the severity of disease symptoms, this would mark covid-19 out as different from influenza, MERS and SARS.

For influenza, a higher infectious dose has been associated with worse symptoms


Citations:

1. https://www.sciencedaily.com/releases/2009/03/090313150254.htm

2. Mark P Zwart, Lia Hemerik, Jenny S Cory, J. Arjan G.M de Visser, Felix J.J.A Bianchi, Monique M Van Oers, Just M Vlak, Rolf F Hoekstra, and Wopke Van der Werf. An experimental test of the independent action hypothesis in virus%u2013insect pathosystemsProc. R. Soc. B, 2009; DOI: 10.1098/rspb.2009.0064

3. https://www.researchgate.net/publication/227225392_Minimum_Infectiv...

4. https://link.springer.com/article/10.1007/s12560-011-9056-7

5. https://www.medrxiv.org/content/10.1101/2020.03.15.20036707v2.full.pdf

6. https://arxiv.org/ftp/arxiv/papers/2003/2003.09320.pdf

Q: How does a living system fight these infections:

Krishna: Living bodies fight infections through their immune system. This immune system has several layers. The first and top layer consists of mechanical barriers, such as the hairs in your nose and the sticky mucus that lines your airways, which prevent pathogens such as SARS-CoV-2, the virus that causes COVID-19, getting to your lung cells.

Next  those lung cells are packed full of “intrinsic” defences that guard against incoming infections. But most viruses capable of infecting people have evolved to get around these defences and can quickly swamp them.

This onslaught triggers the next wave of “innate” immunity. This consists of a rapid, broad-spectrum defence system comprising direct antiviral killing mechanisms or boosted inflammation to kick the virus out.

In most people, this innate response slows down the infection and controls it, allowing the final immune layer – your adaptive immune system – to come into play. Adaptive immunity consists of antibodies made by B cells and antiviral cell-killing T cells.

Both B and T cells develop to fight specific threats, learning on the job during an infection. This response usually takes a bit of time to kick in but has the added benefit that when it is there it can stay around for years, developing a memory of past infections.

This memory is the basis for the effectiveness of vaccines, such as the MMR jab against measles, mumps and rubella. And it is this memory that will be the key to fighting SARS-CoV-2 in the months and years to come.

The problem with obtaining immunity the natural way is that it comes with a significant risk of getting very sick and dying. The realisation of this fact is what drove the first developments of vaccinations, whereby you aim to limit or nearly negate the risk while maintaining the ability to elicit long-term memory immunity.

This video gives a good explanation ...

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