# WHY is SARS-CoV-2 so infectious? **URL:** \ **Category:** The Quarantine Zone\ **Tags:** covid-quarantine\ **Created:** [February 26, 2021, 1:53pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810 "2021-02-26T13:53:00Z")\ **Posts on this page:** 20\ **Page:** 1
**Author:** ![RickJay](https://avatars.discourse-cdn.com/v4/letter/r/bb73d2/32.png) [@RickJay](https://boards.straightdope.com/u/RickJay)\ **Post date:** [February 26, 2021, 1:53pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/1 "2021-02-26T13:53:00Z")
I don’t really understand how viruses work. Could someone explain to me the actual mechanics of why the SARS-CoV-2 virus is more infectious than, for instance, one of the more common influenza strains? ---
**Author:** ![Qadgop\_the\_Mercotan](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/qadgop_the_mercotan/32/83_2.png) [@Qadgop\_the\_Mercotan](https://boards.straightdope.com/u/Qadgop_the_Mercotan)\ **Post date:** [February 26, 2021, 2:02pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/2 "2021-02-26T14:02:13Z")
Good questions, lots of hypotheses, the exact reason still eludes us. Some ideas: 1. Small COVID-19 particles may linger in the air longer than the flu 2. The incubation period for COVID-19 is longer than the flu hence more spreading of it 3. Flu antibodies may last longer than COVID-19 antibodies I’d write more, but I have to go see a patient who has post-acute covid syndrome; still unwell 5 months after his infection. ---
**Author:** ![asahi](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/asahi/32/8693_2.png) [@asahi](https://boards.straightdope.com/u/asahi)\ **Post date:** [February 26, 2021, 2:09pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/3 "2021-02-26T14:09:04Z")
1. Seems to be correct. Aerosolized droplets, particularly in drier air, can remain in the air for hours. Re: 2, you could be right about the incubation period relative to flu - I honestly don’t know. But a related concern is that much of the spread with COVID is asymptomatic. One or two persons with no symptoms at all or mild ones like a sore throat and a periodic light dry cough could walk around shedding virus. We may be looking for obviously ill patients when in fact most people who get the virus aren’t visibly ill for days, if ever. ---
**Author:** ![RickJay](https://avatars.discourse-cdn.com/v4/letter/r/bb73d2/32.png) [@RickJay](https://boards.straightdope.com/u/RickJay)\ **Post date:** [February 26, 2021, 2:57pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/4 "2021-02-26T14:57:05Z")
> [@Qadgop\_the\_Mercotan](#): > > Some ideas: > > 1. Small COVID-19 particles may linger in the air longer than the flu > 2. The incubation period for COVID-19 is longer than the flu hence more spreading of it > 3. Flu antibodies may last longer than COVID-19 antibodies OK but - and if you need to use other examples, go ahead - why can one virus linger longer in the air? Or have a longer incubation period? Like, I’m actually asking, _what about the physical characteristics of a virus would do that?_ Is it the little spiky things, that they are different or more numerous on one virus than another? ---
**Author:** ![Qadgop\_the\_Mercotan](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/qadgop_the_mercotan/32/83_2.png) [@Qadgop\_the\_Mercotan](https://boards.straightdope.com/u/Qadgop_the_Mercotan)\ **Post date:** [February 26, 2021, 3:04pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/5 "2021-02-26T15:04:23Z")
> [@RickJay](#): > > I’m actually asking, _what about the physical characteristics of a virus would do that?_ Is it the little spiky things, that they are different or more numerous on one virus than another? Figure stuff like that out, be a candidate for the Nobel prize, or at least the Lasker award (US version of Nobel for medicine). ---
**Author:** ![RickJay](https://avatars.discourse-cdn.com/v4/letter/r/bb73d2/32.png) [@RickJay](https://boards.straightdope.com/u/RickJay)\ **Post date:** [February 26, 2021, 3:17pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/6 "2021-02-26T15:17:43Z")
There is literally no understanding of how viruses work? ---
**Author:** ![Qadgop\_the\_Mercotan](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/qadgop_the_mercotan/32/83_2.png) [@Qadgop\_the\_Mercotan](https://boards.straightdope.com/u/Qadgop_the_Mercotan)\ **Post date:** [February 26, 2021, 3:34pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/7 "2021-02-26T15:34:46Z")
Now how did you extrapolate to that from my statement? You’re asking some very specific questions about differences in virus transmissibility, in the human body, in the air, in secretions. Viruses are as diverse as mammals, we’re still figuring out the wide range of differences between individual ones, which are discovered in new variations almost daily. We know enough to have our experts build an effective vaccine in less than a year, so I’d say the med/science community knows something. But to expect us to have this new variant, studied for barely a year, fully deciphered in every nuance is asking too much ---
**Author:** ![DesertDog](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/desertdog/32/11503_2.png) [@DesertDog](https://boards.straightdope.com/u/DesertDog)\ **Post date:** [February 26, 2021, 3:50pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/8 "2021-02-26T15:50:21Z")
[Here](https://www.sciencealert.com/a-second-key-used-by-sars-cov-2-to-enter-cells-could-explain-why-it-s-so-infectious) is one take on it from last October. As **QtM** says, it’s an ongoing process and really amazing that vaccines were developed in little more than a year after it was noticed. Compare with Ebola or HIV. ---
**Author:** ![Tfletch1](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/tfletch1/32/5340_2.png) [@Tfletch1](https://boards.straightdope.com/u/Tfletch1)\ **Post date:** [February 26, 2021, 3:51pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/9 "2021-02-26T15:51:19Z")
- Active influenza viruses also linger around in aerosols so I _don’t think_ that their physical characteristics are that different. Studies with masks and on surfaces show that active viruses of both types respond very similarly to these challenges. - It’s looking like antibodies against SARS-CoV-2 hang around in the body for months. Reinfections are typically in people that didn’t have a bad infection in the first place. - The spike proteins on SARS-CoV-2 are different then those on influenza viruses and they use different cellular receptors to attach and enter human cells. That may make a difference since the receptors for influenza are concentrated in cells in the upper respiratory tract whereas the receptors for SARS-CoV-2 are all over the body. - I think the different incubation periods are key. There is a short length of time between being exposed to influenza and experiencing symptoms. Also, people with mild symptoms get over it quickly and are no longer contagious. The incubation time is longer with Covid-19 with people being pre-symptomatic. There may be more people who are completely asymptomatic. That’s particularly true for children and younger adults. Presymptomatic and asymptomatic individuals are contagious which is why the Fauci and CDC changed their stances on masks way back in April 2020. ---
**Author:** ![Qadgop\_the\_Mercotan](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/qadgop_the_mercotan/32/83_2.png) [@Qadgop\_the\_Mercotan](https://boards.straightdope.com/u/Qadgop_the_Mercotan)\ **Post date:** [February 26, 2021, 4:00pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/10 "2021-02-26T16:00:41Z")
Interesting link between high degrees of neuropilin expression in the olfactory epithelium and bulb and COVID’s ability to readily invade this tissue. ACE2 receptors are rather sparse in this area. > **[The role of Neuropilin-1 in COVID-19](https://journals.plos.org/plospathogens/article?id=10.1371%2Fjournal.ppat.1009153)** > > Neuropilin-1 (NRP-1), a member of a family of signaling proteins, was shown to serve as an entry factor and potentiate SARS Coronavirus 2 (SARS-CoV-2) infectivity in vitro. This cell surface receptor with its disseminated expression is important in... The devil is in the details, and man, there are just so many details when you get down to the molecular level of infectious disease. ---
**Author:** ![Tfletch1](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/tfletch1/32/5340_2.png) [@Tfletch1](https://boards.straightdope.com/u/Tfletch1)\ **Post date:** [February 26, 2021, 4:04pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/11 "2021-02-26T16:04:20Z")
> [@Qadgop\_the\_Mercotan](#): > > The devil is in the details, and man, there are just so many details when you get down to the molecular level of infectious disease. Ain’t that the truth! ---
**Author:** ![bordelond](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/bordelond/32/150_2.png) [@bordelond](https://boards.straightdope.com/u/bordelond)\ **Post date:** [February 26, 2021, 5:38pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/12 "2021-02-26T17:38:49Z")
> [@asahi](#): > > But a related concern is that much of the spread with COVID is asymptomatic. One or two **persons with no symptoms at all or mild ones like a sore throat and a periodic light dry cough could walk around shedding virus**. One of the more confounding issues with SARS-CoV-2 is that asymptomatic carriers vary wildly in how much virus they shed. Some shed little to no virus, other shed virions by the billions like a smokestack. I think – but would be pressed to cite – that this is also true of symptomatic carriers. Not that there are symptomatic carriers that never shed virus at any point, but that there is a chaotic, wide range of virus-shedding values among symptomatics. ---
**Author:** ![bordelond](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/bordelond/32/150_2.png) [@bordelond](https://boards.straightdope.com/u/bordelond)\ **Post date:** [February 26, 2021, 5:49pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/13 "2021-02-26T17:49:49Z")
> [@Tfletch1](#): > > - The spike proteins on SARS-CoV-2 are different then those on influenza viruses and they use different cellular receptors to attach and enter human cells. That may make a difference since the receptors for influenza are concentrated in cells in the upper respiratory tract whereas **the receptors for SARS-CoV-2 are all over the body**. A well-supported theory is that [there are SARS-CoV-2 receptors in the walls of arteries (among other organs)](https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2). [Further reading (EMSWORLD, 2/24/2021)](https://www.emsworld.com/article/1225583/covid-19s-relation-myocarditis-ems): > The hypothesis is that COVID-19 enters human cells by attaching the spike protein to the **angiotensin-converting enzyme II** protein membrane, gaining cellular entry. In scholarly articles (and some popular press) about the mechanism of COVID infection, you may see the acronym ‘ACE2’ – that’s the nickname for angiotensin-converting enzyme II. ---
**Author:** ![DSeid](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/dseid/32/20194_2.png) [@DSeid](https://boards.straightdope.com/u/DSeid)\ **Post date:** [February 26, 2021, 10:22pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/14 "2021-02-26T22:22:26Z")
There is of course the most basic reason: the seasonal influenza that most adults see is not as novel as SARS-CoV2 is. Adults have had multiple, even fairly recent, infections with other very similar influenza viruses and also many of them vaccinations as well. Thus in the case of SARS-CoV2 relatively more are susceptible and in each the virus can replicate more vigorously before it is contained both anatomically to the upper tract only and contained to the degree that the individual no longer effectively spreads. In terms of lingering in the air more, why lingering in the air more? Not so much Lasker level - influenza is droplet spread predominantly and SARS-CoV2 has some subset of infected individuals who aerosolize the virus effectively. Of course that just leads to the next question: What about a virus leads some to aerosolize it very well? There are [only a few possibilities](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7719704/): WHERE virus is being released (lower respiratory tract means more aerosolization during normal _breathing_ while upper leads to more with speech and singing; WHEN it is released (presymptomatically and/or asymptomatically when out and about v. only after ill and staying home more likely); and HOW, i.e. the interplay of the virus on individual host factors that cause greater aerosolization. In regards to the last this recent article is very interesting. [https://www.pnas.org/content/118/8/e2021830118](https://www.pnas.org/content/118/8/e2021830118) NHP = non-human primate. > [@](#): > > The generation of respiratory droplets by the breakup of airway lining mucus varies substantially between individuals and with the progression of lung infection. Our findings suggest remarkably similar patterns in two normal human populations in North Carolina and Michigan, and in two kinds of NHP species with two kinds of (viral and bacterial) lung infection. Particularly, that exhaled breath particles in the NHP COVID-19 infection model rise to a crescendo and decrease in size with growth in viral load ([Figs. 3](https://www.pnas.org/content/118/8/e2021830118#F3) and [4](https://www.pnas.org/content/118/8/e2021830118#F4)), and vary between healthy humans in close adherence ([Fig. 1 _A_](https://www.pnas.org/content/118/8/e2021830118#F1)) with classical superspreading 20:80 rules ([13](https://www.pnas.org/content/118/8/e2021830118#ref-13)), suggests that the phenomenon of superspreading of COVID-19 ([15](https://www.pnas.org/content/118/8/e2021830118#ref-15), [16](https://www.pnas.org/content/118/8/e2021830118#ref-16)) may be not only a matter of air currents and proximity of infected and naive hosts but also of phenotype. > > Aging ([10](https://www.pnas.org/content/118/8/e2021830118#ref-10)), diet ([11](https://www.pnas.org/content/118/8/e2021830118#ref-11)), and lung infection ([12](https://www.pnas.org/content/118/8/e2021830118#ref-12)) are all known to promote changes in mucus composition and structure. Phenotypical changes in airway lining mucus, such as variation in surfactant composition and subsurface mucin chemistry, are known to alter mucus−air surface propensity to break up into droplets ([6](https://www.pnas.org/content/118/8/e2021830118#ref-6), [7](https://www.pnas.org/content/118/8/e2021830118#ref-7)), which is consistent with the results shown in [Fig. 2](https://www.pnas.org/content/118/8/e2021830118#F2). … > > … While more research needs to be conducted in human and NHP models, it is possible that a transient effervescence in exhaled respiratory droplets may help explain the limited time window post COVID-19 infection during which infected individuals are most contagious. ---
**Author:** ![Tfletch1](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/tfletch1/32/5340_2.png) [@Tfletch1](https://boards.straightdope.com/u/Tfletch1)\ **Post date:** [February 27, 2021, 2:36am UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/15 "2021-02-27T02:36:17Z")
> [@bordelond](#): > > In scholarly articles (and some popular press) about the mechanism of COVID infection, you may see the acronym ‘ACE2’ – that’s the nickname for angiotensin-converting enzyme II. Yes, and it appears that SARS-CoV-2 utilizes neurophilin-1 as a coreceptor for ACE2 as shown in the paper @Qadgop_the_Mercotan brought over. NRP-1 is involved in vascularization (known as angiogenesis) and the immune system. Patient cadavers who died of Covid-19 had upregulated NRP-1 in a variety of their cells. I’m thinking this has implications for anti-virals that target the interaction of the virus with NRP-1. ---
**Author:** ![Qadgop\_the\_Mercotan](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/qadgop_the_mercotan/32/83_2.png) [@Qadgop\_the\_Mercotan](https://boards.straightdope.com/u/Qadgop_the_Mercotan)\ **Post date:** [February 27, 2021, 2:41am UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/16 "2021-02-27T02:41:15Z")
**DSeid** gives an excellent explanation (as usual) based on the nuts and bolts of what we know or strongly suspect. I am sure ACE2 and NRP will be shown to play some role, but I’d wager there are other critical factors and we don’t understand a tenth of that stuff yet. ---
**Author:** ![DSeid](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/dseid/32/20194_2.png) [@DSeid](https://boards.straightdope.com/u/DSeid)\ **Post date:** [February 27, 2021, 2:44am UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/17 "2021-02-27T02:44:41Z")
> [@Tfletch1](#): > > The spike proteins on SARS-CoV-2 are different then those on influenza viruses and they use different cellular receptors to attach and enter human cells. That may make a difference since the receptors for influenza are concentrated in cells in the upper respiratory tract whereas the receptors for SARS-CoV-2 are all over the body. I’m guessing you need to spell out _why_ having receptors all over may increase infectivity when the portal of entry for both is mostly nasal epithelium, where “the receptors for influenza are concentrated”. ---
**Author:** ![Tfletch1](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/tfletch1/32/5340_2.png) [@Tfletch1](https://boards.straightdope.com/u/Tfletch1)\ **Post date:** [February 27, 2021, 3:07pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/18 "2021-02-27T15:07:09Z")
> [@DSeid](#): > > I’m guessing you need to spell out _why_ having receptors all over may increase infectivity when the portal of entry for both is mostly nasal epithelium, where “the receptors for influenza are concentrated”. You can ask politely. I don’t _need_ to spell out anything. ---
**Author:** ![DSeid](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/dseid/32/20194_2.png) [@DSeid](https://boards.straightdope.com/u/DSeid)\ **Post date:** [February 27, 2021, 3:11pm UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/19 "2021-02-27T15:11:28Z")
No you don’t need to do anything. And I don’t care if you do or you don’t. Personally I understand why. But if you want it to be understood by many others I suspect it won’t be unless you explain why, if that then you’d need to. It isn’t obvious. ---
**Author:** ![Colibri](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/colibri/32/1841_2.png) [@Colibri](https://boards.straightdope.com/u/Colibri)\ **Post date:** [February 28, 2021, 1:32am UTC](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810/20 "2021-02-28T01:32:37Z")
Moved from GQ to the Quarantine Zone. [Next page](https://boards.straightdope.com/t/why-is-sars-cov-2-so-infectious/933810.md?page=2)