The Omicron variant appears to result in less severe Covid-19, giving hope to many people that we’re edging closer to the end of the pandemic war. But it could be the sign of daydreaming amid the nightmare because virulence and transmissibility can be intrinsically linked. To maintain or increase infectiousness, a virus must be virulent. And the next mutation could allow the virus to spread rapidly and cause severe disease at the same time.

Scientists have been monitoring the next SARS-CoV-2 mutation and assessing the nuances in the evolution of virulence. Myxoma virus was the case. The extraordinarily lethal pathogen was released as a bioweapon in Australia to exterminate the rabbit infestation and cause almost 100% death rate. Less virulent myxoma virus evolved, but it continues to circulate and kill rabbits in Australia with a 50% death rate.

However, ample highly virulent myxoma virus strains persist, indicating that evolution toward attenuation did not drive the most virulent variants extinct. The key to maintaining virulence may lie in the inability of myxoma virus to replicate in its insect vectors; high titers of the virus must be maintained in rabbits to ensure transmissibility. Thus, virulence, which achieves high viral load, is critical to its evolutionary success.

The scientists have also been observing the evolution of virulent and transmissible HIV, categorized into two patterns: either burn bright and be brief, or smolder and persist. The former shows virulence and transmissibility are synchronized. The viral load peaks upon initial HIV infection, and then stabilizes when reaching the viral set-point.

The process is variable across infected people, differing by viral variability and individual health. People with higher set-point viral load, left untreated, progress to AIDS more rapidly. Those same people will also be more infectious during this period because higher viral load leads to more viral transmission. By contrast, people with lower set-point viral load will live symptom-free longer and be less infectious over this period.

At the beginning of the Covid-19 pandemic, there was an underappreciation of the rapidity which might determine changes in transmissibility and virulence. That’s why it’s difficult to contain the spread from early on. SARS-CoV-2 variants demonstrate that this virus is repeatedly evolving to be more transmissible, but not all these adaptive variants are demonstrably more virulent.

The Delta variant that dominated global cases in late 2021 shows how SARS-CoV-2 could evolve to be both more transmissible and more virulent, while the Omicron variant is more transmissible but seems less virulent. The Myxoma and HIV findings are relevant to the Covid-19 pandemic, though the mechanisms of SARS-CoV-2 virulence and its relationship with transmission in individuals is unclear.

However, scientists’ assessment of HIV and SARS-CoV-2 outbreaks indicated that immune evasion, receptor binding efficiency, and tissue tropism may contribute to the evolution of virulence. But we need to unfold this correlation in full circle to be able to end the pandemic war with victory to our side.

Credit: https://www.science.org/doi/1