Biology Reference
In-Depth Information
Ascaris and HIV infections leading to impaired CD8
T cell-mediated
control of viral loads, and an alteration in the permissiveness of CD4
þ
þ
T cells to support viral replication, requires elucidation. The effect of
Ascaris co-infection on the chronicity of HIV infection and the develop-
ment of AIDS also needs to be clarified.
Malaria Infection
The prevalence of malaria has declined over the last decade due to
increased awareness and efforts to control and ultimately eradicate this
devastating disease. Despite these efforts, in 2010 there were an estimated
216 million cases and 655,000 deaths as a result of malaria infection. 45
Eighty-six percent of these deaths were in children less than 5 years of age,
who are also at risk for infection and the resultant adverse effects of
Ascaris infection. 45 The pathogenesis of malaria involves a number of
different sequelae including anaemia, metabolic acidosis, respiratory
distress and cerebral malaria, a neuropathy that is often fatal. 46
Malaria infection occurs when female mosquitos deposit the sporozoite
stages of malaria parasite in the dermis of the skin upon feeding.
Although malaria is a systemic infection with malaria parasites repli-
cating within red blood cells (RBC), the parasites undergo a develop-
mental stage in the liver before entering the erythrocytes, replicating
asexually every 48
72 hours depending on malaria parasite species.
Malaria modifies the membrane of parasitized red blood cells (pRBCs), 47
a process that is thought to enhance the adhesive properties of the pRBCs
for endothelial cells and prevent removal of pRBCs from the blood
circulation by the spleen. 48 This process, known as sequestration,
can occur in different organs of the body including the liver, lungs, and
the brain resulting in localized inflammatory immune responses that are
thought to contribute to the pathogenic symptoms of malaria.
Malaria parasites induce pro-inflammatory immune responses typified
by interferon- g (IFN- g ) and driven by CD4
e
Th1 cells. 49,50 This pro-
inflammatory immune response increases the phagocytic activity of
macrophages and drives the production of malaria-specific cytophilic
antibody isotypes, processes that enhance phagocytosis of pRBCs. When
prolonged and/or overexuberant, this inflammatory immune response
can contribute to the pathogenesis of malaria. However, asymptomatic
malaria infections are common in endemic areas and are thought to occur
because pro-inflammatory immune responses are balanced by the
induction of the immunoregulatory cytokines (IL-10 and TGF- b ). 49
In Asia, Ascaris co-infection has been reported to have protective
effects against cerebral malaria 6,7 as well as jaundice and renal failure
in malaria-infected individuals. 51 Animal models have shown that
immunoregulatory cytokines are essential for protecting against the
þ
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