General update, April 19

Posted on by

1. A study from Italy.

We found no statistically significant difference in the viral load (as measured by genome equivalents inferred from cycle threshold data) of symptomatic versus asymptomatic infections

Pointer from Megan McArdle.

Although the margin that I care about is mild vs. severe rather than symptomatic vs. asymptomatic, this is somewhat discouraging for those of us who would like to believe that getting the virus in low amounts would be ok.

Note the the study measures viral load among people after they have the virus, not viral load at onset. I think the only way to make guesses about viral load at onset is to do case studies that look at how people got the virus.

I think that what this study strongly reinforces is the hypothesis of asymptomatic spreading.

2. A case study that suggests being in the path of airconditioning flow and an asymptomatic spreader gave people the disease.

I now think that these sorts of case studies are going to be the best way to gather useful evidence about the virus. I would especially like to see case studies that can help assess whether there is anything we can do to affect whether one gets a mild or severe case.

5 thoughts on “General update, April 19”

  2. “this is somewhat discouraging for those of us who would like to believe that getting the virus in low amounts would be ok.”

    We know that variolation worked (that is, produced milder symptoms and reduced smallpox fatality levels from 1/3 to 1/100, though not to 1/M, like a vaccine), and whether or not that study is discouraging depends on the mechanism of how it works.

    If variolation works by reducing peak (or “set point” equilibrium) viral loads, then the study is discouraging, because viral loads and symptoms seem uncorrelated.

    On the other hand, if variolation works by reducing symptoms, because viral load didn’t get too far ahead of the immune system in their respective ramp-ups, then the study is neither discouraging nor encouraging.

    None of the young kids they tested had any load at all, even those that lived with infected people. Unfortunately they didn’t test for antibodies. So we don’t know if the kids had it first, and got over it, or if, despite presumably high initial exposures, they never got it at all, because even at that high level, their young, strong immune systems totally knocked it out early.

    • Here’s an article from The Lancet from a study in Hong Kong, Temporal profiles of viral load … during infection by SARS-CoV-2

      Figure 3A shows:

      1. Reasonably confident positive relationship between age and peak viral load – consistent with typical results in immunosenescence.
      2. No significant relationship between peak or initial viral load levels, on the one hand, and whether one has a mild or severe case on the other hand. “our study only showed that the median viral load was 1 log10 higher in severe cases than in mild cases, and the difference was not significant”

      Figure 4 shows bursts of antibodies against both “RBD” (the receptor binding domain of the spike surface protein), and “NP” – The cv19 internal nucleoprotein, which are both targets for vaccine efforts.

      This stood out to me:

      For most patients, the viral load of SARS-CoV-2 was very high at presentation and declined steadily. Despite development of antibodies against surface and internal proteins of SARS-CoV-2, viral RNA could still be detected in posterior oropharyngeal (deep throat) saliva samples from a third of patients for 20 days or longer. Peak viral load correlated positively with age. Most patients had an antibody response at 10 days or later after onset of symptoms.

      That puts a different twist on the question of whether certain health care resources might be overwhelmed. In particular, if some patients don’t clear the virus for weeks and shouldn’t be released from medical isolation until they clear, then if the supply of special isolation beds is inelastic, you can only hold so many patients at once. Hospitals may be releasing people who have gotten better, and asking them to self-quarantine at home, but they aren’t using PCR tests as a threshold (not enough tests anyway), so those people may still be spreading, even if they would test positive on antibody tests. Yikes.

      Here’s another one:

      The viral load profile of SARS-CoV-2 is similar to that of influenza, which peaks at around the time of symptom onset, but contrasts with that of SARS-CoV at around 10 days and that of MERS-CoV at the second week after symptom onset. The high viral load on presentation suggests that SARS-CoV-2 can be transmitted easily, even when symptoms are relatively mild. This finding could account for the efficient person-to-person transmission noted in community and health-care settings. Clusters in families, workplaces, religious gatherings, and food premises have been widely reported.

  4. Sadly, the case study in #2 is misleading in its title. The transmission was not due to air conditioning except that air conditioning has fans that create airflow. The study only describes downwind transmission at distances greater than the “spittle into your mouth and nose” social distancing recommendations. This is consistent with studies on the transmission of influenza back to 1941, that took efforts to impede droplet transmission.

    There are actually few US studies on the transmission of respiratory viruses even though influenza kills tens of thousands of Americans each year.

    I believe restaurants are going to have to look into creating negative-pressure ventilation in their dining areas. This will likely require an additional exhaust vent to avoid creating a flow throughout the space to the kitchen exhaust vents. This will increase energy costs associated with hvac and require changes in energy-efficiency building regulations.

Comments are closed.