From the beginning of the SARS-CoV-2 epidemic it has become apparent that there is great heterogeneity in transmission.
Some patients do not transmit it at all while others transmit it to too many.
Heterogeneity in transmission is something we have known well about coronaviruses of this order for about 15 years.
But what are the biological factors that determine this heterogeneity?
Professors of the Medical School of the National and Kapodistrian University of Athens, Gikas Majorkinis and Thanos Dimopoulos (Rector of EKPA) report that a much-discussed hypothesis is the viral load, ie the amount of virus excreted in the upper respiratory tract (nasopharynx).
The example of HIV
Viral load as a measure important for the transmission and severity of the disease is widely used in the monitoring of HIV patients.
In this case the viral load in the blood shows how contagious the patient is while the levels of viral load in the blood after the first phase of the infection are indicative of how fast the disease will progress. By reducing the viral load in the blood achieved with modern therapies, carriers can live normally while ceasing to be contagious.
What applies to the load on the SARS – CoV-2
In contrast to viral load in the blood, measuring viral load in respiratory samples presents many problems. In principle, it is difficult to compare samples collected in different ways. In contrast to blood sampling, upper respiratory sampling varies widely in the collection of biological material.
The other characteristic problem in the comparability of samples from different patients is due to the fact that the amount of virus (SARS-CoV-2) secreted at different stages of the disease changes dramatically within hours and from day to day. It is typical that in the same day in a patient's sample the density of the virus can increase millions of times. It is therefore extremely difficult to find a way to reliably compare samples from different patients so that all studies that compare viral loads between patients suffer from sampling comparability problems.
Viral load in relation to variants and vaccination history
A recent publication in the prestigious New England Journal of Medicine presents for the first time data that take into account and control the variation of patient sampling in terms of viral load. This was made possible by repeated sampling of subjects who were monitored for a long time before becoming ill.
This made it possible to measure the viral load before the onset of symptoms and until the virus escaped from the patients, now recording virus load curves per patient. Then instead of comparing a viral load value per patient they compared the viral load curves. What became apparent from this comparison is that the total virus excretion between the different strains analyzed (Alpha, Delta, original strains) did not differ significantly.
Any differences that had been observed in previous studies were likely due to systematic errors during sampling and the phase of the epidemic curve of each strain. The most interesting element, however, emerged when the viral load curves were compared between vaccinated and unvaccinated individuals.
In this case the difference was characteristic and significant, with the virus response time being significantly shortened in vaccinated compared to non-vaccinated showing that the time transmitted by vaccinated is significantly shorter.
in.gr
