Destroying T-cells in a different way in .NET

Drawing QR Code in .NET Destroying T-cells in a different way

HIV disease progression can vary dramatically from patient to patient, and evolution does not occur along exactly the same trajectory in each case But one major event which is observed repeatedly is the evolution of viruses later in infection that attack the immune system in a different way These viral variants (called X4 variants) are able to attach to a different part of the surface of immune cells (a cellular feature called the CXCR4 receptor ) and destroy the T cells in a different way The X4 type begins to increase in frequency around the time that the overall genetic diversity of the viral population is decreasing, and the peak of the X4 virus type is associated with period proceeding transition to full blown AIDS symptoms Researchers don t completely understand how theses X4 viruses influence the disease or whether the X4 variants evolve in every patient What they do know is that the X4 variants cause T cell death differently from the original variants

HIV is as interesting as it is scary Consider this to be the section of other cool things about the human immunodeficiency virus if you can use the word cool when talking about a deadly pathogen If you can t, consider this to be the section of noteworthy-but-not-vitally-important information for serious-minded readers

During the initial infection, the virus binds to a CCR5 co-receptor (refer to Attacking T cells, earlier in this chapter) As it turns out, not everyone has that same molecule Some people have a mutation that makes a slightly different CCR5 molecule People who have one mutated copy of the CCR5 locus show delayed progression toward full-blown AIDS And people who have two mutated copies appear to be resistant to HIV infection Interestingly, this mutation is found primarily in Europe, and its prevalence is correlated with the degree to which a particular location experienced plagues in the past It s been hypothesized that this mutation may have made people more resistant to certain other disease organisms and that as a result the mutation increased in frequency in places that once experienced plague Just by coincidence, the same mutation confers resistance to HIV infection Scientists aren t sure that the bubonic plague was caused by black-plague bacteria Instead, it may have been caused by a viral hemorrhagic fever

Evolution within the patient selects for a more divergent virus, and that viral diversity increases through time in the individual (refer to the earlier section HIV Evolution within the Patient ) When you compare the virus present during the initial period of infection across different people, however, you find less divergence among people than you see over time within one person Think about this for a minute: If the virus is diverging in one person, and that person infects a second person, you d expect that the second person would start out with a more divergent population of the initially infecting virus But that s not the case Here s why: After infection, strong selection for the ancestral viral type occurs, so the virus evolves back toward this condition This selection may happen for at least a couple of reasons:

The viral forms present in a person late in the infection may not be well suited to living in the environment present in a newly infected person Hence, selection favors going back to an initial viral form Although the diverse viral population may be perfectly capable of surviving in a newly infected host, this population may be outcompeted by viral variants that have mutations resurrecting the ancestral type

One way that the HIV population generates all that diversity is via a huge amount of recombination among viruses In recombination, a DNA or RNA sequence (whichever the critter uses for genomic information) is produced that s a combination of two original sequences For most organisms, recombination is generally believed to happen far less frequently than mutation But in HIV, the recombination rate may approach the rate of mutation Scientists know about the recombination rate by making and analyzing phylogenetic trees for a group of viruses with different genes For organisms with low rates of recombination, phylogenies constructed from different genes should have trees that match The extent to which they don t match allows scientists to determine the frequency of recombination When you take a bunch of HIV viruses, determine the sequence of several genes, and then make phylogenetic trees from these different genes, the resulting trees don t always match This shows that, rather than being a rare event, recombination is a major source of the diversity in the HIV population within a patient