The evolution of the HIV population appears to contribute to the death of the ho

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The evolution of the HIV population appears to contribute to the death of the host in at least three ways. First, the continuous evolution toward novel epitopes enables the viral population to stay far enough ahead of the immune response to avoid elimination. Second, the viral population within many hosts evolves toward ever more aggressive replication. Ryan Troyer and colleagues (2005) took sequential HIV samples from several untreated patients. The researchers grew the virions from each sample on white blood cells from an uninfected donor. To each culture dish, the researchers added one of four control strains of HIV against which the2 virions from the patient would have to compete. In each dish, the viral strain that could replicate most efficiently became numerically predominant. Troyer and colleagues assessed the competitive fitness of the virions from the patients' samples based on their overall performance against the four control strains. The results appear in Figure 1.29. Each color represents the sequential samples from a Figure 1.29 HIV populations particular patient. In seven of eight cases, the competitive fitness of the patient's In many hosts evolve toward virions steadily increased over time. The longer a patient harbors an HIV popula- more aggresslve replcation tion, the more damaging the virions in the population become 40 80 120 Months since first positive HIV test rs an FHIV popu Redrawn from Troyer et al. (2005) Third, in at least half of all hosts, strains of HIV evolve that can infect naive T cells (Shankarappa et al. 1999; Moore et al. 2004). An HIV virion's ability to infect a given cell type is determined by the coreceptor the virion uses. Early in most HIV infections, most virions use CCR5 as their coreceptor. CCR5 is tound on macrophages and on regulatory, resting, and effector I cells (see Figure 1.6). As the infection progresses and the HIV population evolves, virions often emerge that exploit a different coreceptor. These strains, called X4 viruses, use a protein called CXCR4. CXCR4 is found on naive T cells. Hosts without X4 virions 600 Because naive T cells are the progenitors of memory and effector T cells, the emergence of virions that can infect and kill naive T cells is typically bad news for 400 the host. Hetty Blaak and colleagues (2000) sampled the viral populations of 16 * HIV patients to determine whether they contained X4 virions. Then, for a time 200X4 virions span running from a year before to a year after the date of this sample, the re- searchers calculated the average helper T-cell counts in the blood of patients with X4 viruses versus the patients without. The results appear in Figure 1.30. The Flgure 1.30 HIV strains that average T-cell counts in the patients without X4 viral strains held fairly steady use CXCR4 as a coreceptor has- over time; the average counts in the patients with X4 strains fell. When virions ten the collapse of their hosts arise that undermine the immune system's ability to replenish its stock of T cells, they apparently accelerate the immune system's demise Hosts with 12 18 24 Time (months) immune systems Redrawn from Blaak et al. (2000) The evolution of the HIV population within a host is shortsighted (Levin and Bull 1994; Levin 1996). The virions do not look to the future and anticipate that as their population evolves, i will ultimately kill its host. Virions are just tiny, A second possible reason HIV unthinking, molecular machines. Evolution by natural selection does not look to infection is fatal: During an the future either. It just happens automatically infection, the viral population evolves--to evade the immune system, replicate more rapidly and use a different coreceptor A Surprising Clue Besides abetting the lethality of HIV infection, evolution within hosts has given researchers an unexpected clue to another contributory factor. This clue was un- covered by Philippe Lemey and colleagues (2007). Lemey reanalyzed an extraor-

Explanation / Answer

The correct answer is B) Statement iv inaccurately completes the sentence.

Explanation : The option iv states that in case of patients where HIV strains evolved to become X4 viruses led to higher T cell count than the patients who still had unevolved or ancestral HIV population. This statement is incorrect.

Scenario 1 : The ancestral HIV population which uses CCR5 as a co-receptor can infect the effector T-cells. If this happens, Naive T cells which are the originators of these effector T cells will replenish and make up for the loss of the infected T cells. In other words, the infected effector T cells can be replaced by newly formed effector T cells from their progenitors (Naïve T cells). So there will be replenishment of T cells in this case.

Scenario 2 : However, the HIV strains which have evolved to become X4 viruses use a different co-receptor, a CXCR4 instead of the primitive CCR5. This allows the X4 strains to infect the originators Naive T cells itself. So now, in the absence of proper functional originators, there would be no effector T cells in question to replenish the infected cells as in scenario 1.

So in conclusion, the CD4 T cell count in patients containing X4 viruses would be much lower as compared to the cell count in patients with ancestral HIV population. X4 debilitates the immune system's ability to replenish the lost T cells.

The statement iv however states the exact opposite.

  

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