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The secret origin of SIV: Why are African apes the virus' reservoir?
Simian immunodeficiency virus (SIV) is a retrovirus of the genus Synechovirus that is known to cause persistent infection in at least 45 species of non-human primates. Recent studies suggest the virus has been present in monkeys and apes for at least 32,000 years, and possibly longer. The human immunodeficiency virus (HIV) corresponding to SIV, such as HIV-1 and HIV-2, was transmitted to humans through interspecies leap, which has prompted scientists to think deeply about the origin and history of SIV.
Analysis of samples from four species of Bioko monkeys suggests that SIV may have begun infecting the monkeys tens of thousands of years ago, when they were cut off from the mainland by rising sea levels.
The study showed that SIV was identified from three primates, SIVsmm (vervet monkeys), SIVgor (gorillas) and SIVcpz (chimpanzees), and was transmitted through hunting and eating their blood. And the transmission to humans is what causes HIV-2 and HIV-1. However, these non-human hosts have demonstrated amazing adaptability in coexisting with SIV; unlike HIV infection in humans, many SIV infections are non-pathogenic in their hosts.
Studies have found that in some natural host species, regulation of CCR5 co-receptor activity is one of the natural strategies to avoid disease.
Chimpanzees in Africa display similar symptoms to SIVcpz infection, developing AIDS-like symptoms similar to HIV-1, which also emphasizes the differences in variability and adaptability between different hosts.
Virology and Host Relationship
The molecular structure of SIV is similar to that of HIV, both of which are positive-sense single-stranded RNA viruses that replicate and transcribe in a specific manner within host cells. However, the host of this virus can withstand infection by its pathogen without developing a condition similar to HIV. This is related to the genetic adaptation of non-human hosts, such as African green monkeys, which have evolved to adapt to SIV and rarely develop chronic infection.
The study pointed out that the rapid reproduction and transcriptional inaccuracy of SIV lead to the emergence of antigenically different variants in the host, and the impact of these variants on the immune system during the evolution process is crucial.
The data also show that the course of SIV infection in nonhuman primates differs significantly from the course of HIV infection in humans. Depending on the interaction between different SIV variants and the host, chronic immune activation does not occur in many infected individuals.
Infection and Ecology
When mapping the epidemiology of SIV, researchers found that chimpanzee populations in certain African regions are suffering from SIV, which may be related to local ecological changes. In addition, SIV does not cause significant individual mortality in its native habitat, which makes the virus's infection and pathogenic mechanisms in the host stand in stark contrast.
It has been reported that SIV infection is very common in African green monkey populations, but these viruses do not affect the overall survival and reproduction capacity of their hosts.
More profound is how SIV can evade evolution and host immune response in different environments and interactions with humans, so that it can form a stable symbiotic relationship in certain populations, which has aroused great concern. Discussion of future vaccine development.
Future research directions and challenges
How to understand and use this knowledge to combat the HIV epidemic in humans has also become an important research area. With the progress of vaccine research and development, scientists hope to help humans overcome the challenges of HIV-1 in the future. Further research into SIV and its host adaptation mechanisms may reveal critical information that will allow scientists to develop more effective prevention and treatment strategies for the HIV epidemic.
However, more in-depth research is still needed to explain how humans can adapt to SIV or similar viruses to avoid possible epidemic challenges in the future.
This knowledge about SIV not only clarifies the origin of human immunodeficiency virus, but also triggers a new round of thinking: in the face of a constantly changing viral environment, how do we adjust our research and prevention strategies to avoid emerging viruses? The emergence of disease?
