Reminders of known info (due to pre-publication):
The virus replicates in your throat in early stages of the sickness, and later attacks your lungs. Sore throat? Stay home. Mild symptoms? Stay home!
https://www.nature.com/articles/s41586-020-2196-x
From the abstract:
COVID-19 can present as a mild upper respiratory tract illness. Active virus replication in the upper respiratory tract puts the prospects of COVID-19 containment in perspective.
From the paper:
The clinical courses in subjects under study were mild, all being young to middle-aged professionals without significant underlying disease. Apart from one patient, all cases were first tested when symptoms were still mild or in the prodromal stage, a period in which most patients would present once there is general awareness of a circulating pandemic disease
Translation: all were otherwise fit and healthy and were just a little sick - just that amount they would probably contact a medical professional now.
Critically, the majority of patients in the present study seemed to be
already beyond their shedding peak in upper respiratory tract samples
when first tested, while shedding of infectious virus in sputum con-
tinued through the first week of symptoms. Together, these findings
suggest a more efficient transmission of SARS-CoV-2 than SARS-CoV
through active pharyngeal viral shedding at a time when symptoms
are still mild and typical of upper respiratory tract infection. Later in
the disease, COVID-19 then resembles SARS in terms of replication
in the lower respiratory tract. Of note, the two patients who showed
some symptoms of lung affection showed a prolonged viral load in
sputum. Our study is limited in that no severe cases were observed.
Emphasis mine. Translation: ALL of them were infectious before they would have contacted a medical professional. This is a difference to the old SARS virus which makes it more contagious. The later stages are just as deadly. The research here has only been conducted on generally mild cases, we need more severe cases studied to be able to say more (e.g., about how long someone stays infectious in severe cases, since the data here leaves the possibility open that severe cases are infectious for a longer than usual period.).
The combination of very high virus RNA concentrations and occasional detection of sgRNA-containing cells in stool indicate active replication in the gastrointestinal tract. […] Our failure to isolate live SARS-CoV-2 from stool may be due to the mild courses of cases, with only one case showing intermittent diarrhea
Translation: I shit you not, like in the old SARS, it seems your shit might just as well be infectious. (But the scientific jury is still out on that!)
The prolonged viral shedding in sputum is relevant not only for hospital infection control, but also for discharge management. In a situation characterized by limited capacity of hospital beds in infectious diseases wards, there is pressure for early discharge following treatment. Based on the present findings, early discharge with ensuing home isolation could be chosen for patients who are beyond day 10 of symptoms with less than 100,000 viral RNA copies per ml of sputum. Both criteria predict that there is little residual risk of infectivity, based on cell culture.
Translation: the virus can be detected in your spittle even while you are still getting better, but seems not to be infectious. We can use the concentration in your spittle to decide when we can send you home, early, under a strict quarantine which you are not going to break FFS to free beds we desperatly need to treat other cases.
Seroconversion in most cases of SARS occurred during the second week of
symptoms. […] When aligned to viral load courses, it seems there is no abrupt virus
elimination at the time of seroconversion. Rather, seroconversion early
in week 2 coincides with a slow but steady decline of sputum viral load.
Neutralization testing is necessary to rule out cross-reactive antibodies directed against endemic human coronaviruses. […]
Translation: your immune system is kicking in about one week after you start feeling very slightly sick, but the virus is still there and we can detect it in your spittle. See above. That your immune system is responding about two weeks after infection is great news, because we can then detect the virus indirectly based on antibodies which is much, much easier PLUS its possible on a larger scale than what we are doing now (i.e., directly measuring the concentration of the virus). We need to be bloody careful with this and test for specific antibodies to this virus because there are common relatives and we must not have false positives (because you then would still be able to catch the bugger!).
Based on frequently low neutralizing antibody titers observed in coronavirus infection, we have here developed a particularly sensitive plaque reduction neutralization assay. Considering the titers observed, a simpler microneutralization
test format is likely to provide sufficient sensitivity in routine application and population studies.
Translation: we already have a very sensitive test in our research lab which tells us if you have been infected and your immune system did kick in. Based on what we saw, we think someone in the industry can design a test for large-scale antibody testing!
Please note: I omitted much, and translated to the best of my understanding. I am not a medical professional, nor a virologist.
But I know a good study when I see one.
FTR, this is already older than a month. The scientific community actually working on SARS CoV 2 knows these results. Now, a broader scientific audience knows, too.
Also, please see over here:
