Final answer:
Beneficial T-to-I mutations in SARS-CoV-2 may help the virus evade the immune system, increase infectivity, or adapt to different human populations, much like the CCR5-∆32 mutation offers HIV resistance in humans.
Step-by-step explanation:
The evolutionary advantages of T-to-I (thymine to inosine) mutations in SARS-CoV-2, which are the result of RNA editing processes, can confer benefits similar to those seen with beneficial mutations in humans. For example, the CCR5-∆32 mutation provides resistance to HIV by inhibiting the virus's ability to enter T-cells. Similarly, SARS-CoV-2 mutations could potentially enhance the virus's ability to evade the host's immune response, increase its infectivity, or allow it to better adapt to different human populations.
Mutations in viruses, just like in humans, can confer certain advantages. The Trade-Off Hypothesis discusses the balance between virulence and transmission, where an evolutionarily successful pathogen must be capable not only of infecting a host but also of spreading to new hosts. Mutations that facilitate this process - whether by avoiding detection by the host immune system or by increasing the rate of replication - provide a clear adaptive advantage in the evolutionary arms race between pathogens and their hosts.
Beneficial mutations in viruses act as a driving force in their evolution, increasing the likelihood of the mutated virus surviving and reproducing within its host environment. These mutations can arise by chance and may become more widespread if they contribute positively to the virus's reproductive success.