Biology Reference
In-Depth Information
and intestine,
29
particularly if larval migration leads to physical damage
of the epithelium of the lung tissue.
EFFECTS OF ASCARIS ON SYSTEMIC
CO-INFECTIONS
The most likely explanation for interactions with Ascaris and
co-infecting systemic pathogens is via immune modulation. Here we
focus on the two most common systemic infections likely to be found
in Ascaris-infected individuals, HIV and malaria.
HIV Infection
Although there is a growing body of reports confirming the presence of
individuals co-infected with HIV and Ascaris, there has been relatively
little work done into the effects of co-infection on HIV and Ascaris infec-
tion. Over 30 million people are infected with HIV globally, and 22 million
people are estimated to be co-infected with helminth infections and
HIV.
30,31
HIV is a retrovirus that causes acquired immunodeficiency
syndrome (AIDS). There are two related retroviruses, HIV-1 and HIV-2;
HIV-1 is the most predominant strain and HIV-2 is more localized to
West Africa. Infection with HIV occurs via transmission in bodily fluids,
in particular semen, vaginal secretions, and blood. HIV causes inflam-
mation of the GI tract leading to destruction of enterocytes and a break-
down in the integrity of the epithelial surface.
32
The main site of HIV replication in the body is CD4
Tcells expressing
CCR5, although other cell types including monocytes/macrophages and
dendritic cells can be infected and contribute to reservoirs of latent virus
in the body.
33
HIV is an enveloped retrovirus that contains two copies of
the viral genome and transcription factors required for reverse tran-
scription of RNA into cDNA, a necessary prerequisite for integration into
the host DNA. The amount of detectable viral load in the plasma is
correlated with the proliferation of the virus in CD4
þ
T cells. HIV is
integrated into the genome of infected cells as a provirus and the repli-
cation is controlled by a number of transcription factors which bind to the
long terminal repeat (LTR) region of the virus upregulating or down-
regulating viral gene expression and replication.
34
HIV is capable of
replicating in proliferating CD4
þ
T cells, including undifferentiated Th0
cells and Th2 cells,
35
utilizing a plethora of transcription factors involved
in transcribing genes required for T cell proliferation to replicate.
In general a Th1 response is necessary to provide help for full activation
of viral-specific CD8
þ
cytotoxic Tcells to induce apoptosis in HIV-infected
þ
CD4
T cells, controlling viral
loads and infection (for review see
þ
