mRNA vaccination found to reduce COVID-19 infectious viral load

mRNA vaccination found to redu...
New research found three vaccine doses were crucial in reducing infectious viral load following a breakthrough infection with the Omicron variant
New research found three vaccine doses were crucial in reducing infectious viral load following a breakthrough infection with the Omicron variant
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New research found three vaccine doses were crucial in reducing infectious viral load following a breakthrough infection with the Omicron variant
New research found three vaccine doses were crucial in reducing infectious viral load following a breakthrough infection with the Omicron variant

New research published in Nature Medicine has found COVID-19 vaccination can reduce a person’s infectious viral load. The study compared the infectiousness of different SARS-CoV-2 variants between vaccinated and unvaccinated subjects.

We know the virus that causes COVID-19 initially takes hold in a person’s upper respiratory tract. In the early days of infection the virus rapidly replicates and this is the point when a person is most infectious.

The volume of virus in a person’s upper respiratory tract is generally referred to as a viral load. A high viral load is believed to be associated with greater infectiousness, and researchers have two main ways of measuring the volume of that viral load. The first, and most commonly used method, comes from tracking a specific PCR (polymerase chain reaction) testing metric.

A PCR test works by amplifying copies of the virus’ genetic material. Each cycle of the test basically doubles the genetic material present in the individual sample. Usually, if no trace of virus has been found after 30 to 40 cycles a PCR test is reported as negative.

The CT (cycle threshold) value is a measure of how many times the test cycles before finding viral genetic material. A low number means there was plenty of viral material in the original swab sample, while a higher CT value means the opposite.

So CT values are often used to determine the viral load of a COVID-19 patient, and a high viral load is generally considered to correlate with the contagiousness of a given patient at that point in time. However, research linking PCR measured viral loads and transmission has been inconsistent. Isabella Eckerle, lead researcher on the new study, says measuring viral load this way is not a good indication of how infectious that specific viral load is.

“[A PCR] test is very effective in identifying infected people, but does not indicate whether they are infectious, that is, capable of transmitting the virus to other people," explained Eckerle. "However, the notion of contagiousness is essential for deciding on collective prevention measures, such as periods of isolation."

The second way of measuring the infectiousness in a given viral sample is by isolating that virus in cell cultures and watching how rapidly it replicates. This method has been used for many years as a good measure for viral infectiousness, but it hasn’t been frequently deployed in the COVID-19 pandemic. Current safety measures require this kind of test with SARS-CoV-2 to be conducted in a biosafety level 3 laboratory. Not an easy process to routinely perform.

The new research set out to perform these tests on several hundred samples of SARS-CoV-2 including three different variants (the original strain, Delta and Omicron) spanning both unvaccinated and vaccinated infections.

The researchers first found there was very little correlation between viral load as measured by PCR CT value and infectious viral load measured from cell cultures. The researchers also found age and sex played no part in influencing a person’s infectious viral load.

“Next, we have investigated the effect of vaccination (2 doses mRNA) on infectious viral load,” Eckerle reported on Twitter. “In vaccinated individuals with a Delta breakthrough infection, infectious virus was almost 5-fold lower & was cleared more rapidly than in the unvaccinated with Delta.”

The results were quite different when the researchers looked at infectious viral loads in patients with the Omicron variant. With Omicron, those two-dose vaccinated patients were found to have similar infectious viral loads to unvaccinated patients. But a big drop in infectious viral load came with the third vaccine dose. This matches a large volume of research finding a third vaccine dose is crucial in protecting against the Omicron variant.

“This is immunologically consistent: many vaccines require 3 doses spaced several months apart to induce a sustained immune response, such as that against Hepatitis B virus," explained Eckerle.

One of the more unexpected findings in the new study was the observation that, overall, it seems the Omicron variant generated lower levels of infectious viral load compared to the Delta variant. Considering we know Omicron to be significantly more transmissible than previous SARS-CoC-2 variants the researchers conclude it is still unclear exactly what mechanism is behind the variant's increased transmissibility.

“We still don't know, but our data suggest that other infectious mechanisms are at play," said study co-author Pauline Vetter. "It is now clear that the mutations of Omicron strongly differentiate it from other variants, allowing it to partially escape the vaccine, and diminish the effectiveness of some antiviral treatments used so far."

While the study cannot explicitly associate real-world transmissibility to this cell cultured metric of infectious viral load, the findings do offer insights into how vaccination affects infectious viral load. Eckerle hopes the study influences public health decisions as she believes the findings do suggest, even in the face of Omicron, vaccination is likely an important factor in reducing rates of transmission.

“… vaccination can reduce infectious viral load, likely leading to lower onward transmission,” Eckerle said on Twitter. “These findings underscore the benefit of vaccination on SARSCoV2 circulation beyond individual protection from severe disease.”

The new study was published in the journal Nature Medicine.

Source: University of Geneva

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