HIV and TB and iron excess

HIV and TB and iron excess

Necrosis of host cells and survival of pathogens following iron
overload in an in vitro model of co-infection with human
immunodeficiency virus (HIV) and Mycobacterium tuberculosis.
Traoré HN, Meyer D
Int J Antimicrob Agents. 2007 Jan 19;

Mycobacterium tuberculosis, human immunodeficiency virus (HIV) and iron
overload (dietary/hereditary) are very common in sub-Saharan Africa.
The requirement for iron as a crucial factor for cellular processes is
well established, as are the disadvantages of excess iron in the
system. Mycobacterium tuberculosis and HIV are believed to have a
reciprocal effect on each another. An in vitro model was evaluated
where chronically HIV-infected cells were secondarily exposed to M.
tuberculosis in the presence of iron overload. Co-infection alone
caused cell type-specific reductions in host cell viability, more than
doubled the number of viral particles and stimulated bacterial
viability. Excess iron (in addition to co-infection) further decreased
cell viability, with a marked increase in necrosis (rather than
apoptosis) of cells, and was also found to enhance both HIV (26%;
P<0.01) and M. tuberculosis (47%; P<0.01) replication. Chelation of
excess iron with deferoxamine abrogated the enhanced replication of the
pathogens, with a marginal restoration in host cell viability. These
findings demonstrate that (i) increased levels of iron in HIV-infected
patients secondarily co-infected with M. tuberculosis elevate viral
replication, which could lead to rapid disease progression, and (ii)
iron chelation may serve as a means to slow/decelerate these processes.

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