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Hersperger et al. 36 ). During acute HIV infection, most CD4
T cells are
depleted from the GI tract, a phenomenon that persists throughout chronic
infection. In the periphery CD4
þ
T cell numbers initially recover but
during the chronic phase of HIV infection CD4
þ
T cells are gradually
depleted with continued viral replication over a number of years.
The impact of Ascaris infection in HIV-infected individuals is currently
unclear. Immune activation is essential for CD8
þ
T cell-dependent viral
control but it is also associated with viral replication and progression to
AIDS. Given this dichotomy, possible effects of Ascaris co-infection on
HIV infection are numerous, and likely to depend on the order and timing
of co-infection.
The immune response generated by Ascaris infection biases CD4
þ
T
cells towards a Th2/immunoregulatory (Treg) phenotype. Both Th2 cells
(a source of IL-4) and T reg cells (a source of IL-10 and TGF- b ) antagonize
the development of Th1 cells. 37 It could be argued that established Th2 and
immunoregulatory immune responses generated by an Ascaris infection 11
may be associated with HIV progression in Ascaris/HIV-co-infected
individuals by antagonizing the development of Th1 cells that can provide
help for CD8
þ
T cell-mediated control of viral loads ( Figure 4.2 ). In
support of this theory anthelmintic treatment of individuals with intestinal
helminth/HIV co-infection has been associated with a decreased viral load
in one study 38 and in another study a trend towards decreased viral load
was associated with a statistically significant increase in CD4
þ
T cell
counts in albendazole-treated individuals compared with untreated indi-
viduals. 8 Although no obvious changes in serum cytokine responses
were apparent before and after treatment in the latter study 39 there was
a marginal, but statistically significant, reduction in IL-10 production after
treatment for intestinal helminth infection. This suggests that IL-10
generated by an Ascaris infection could be detrimental to HIV control.
However, it is possible that immunosuppressive immune responses
generated in Ascaris infection may have a profound effect on viral loads
and HIV progression without effects of immune control mechanisms. Th1
cells have been shown to be less permissible to viral replication than Th0
or Th2 cells. 35,40 It is therefore feasible to speculate that increased viral
loads described in the above study 8 may have arisen because activation
and expansion of Th2 cells by Ascaris co-infection in the gut-associated
lymphoid tissue increased resources for viral replication.
Not all studies agree that helminth infection exacerbates viral loads in
HIV co-infected individuals. Modjarrad et al. 41 did not find any effect of
intestinal helminth treatment on viral loads in an HIV-infected population
co-infected with Ascaris and hookworm. Helminth infection may even, in
some cases, protect against the effects of HIV infection. In one study
Schistosome/HIV co-infected individuals had higher CD4
þ
T cell counts
compared with HIV singly-infected individuals, a finding that was
þ
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