The Human Immunodeficiency Virus (HIV) is classified into
two types (HIV-1 and HIV-2). Although these two types of
HIV (HIV-1 and HIV-2) cause essentially the Acquired Immune
Deficiency Syndrome (AIDS); there are major differences between
them. Their phylogenies, pathology, virulence, developments,
modes of transmission, infectivity and epidemiology
differ [2]. Compared to the HIV-1, the HIV-2 has a slower
progression to AIDS stage and is hardly transmitted [2]. Coding
regions of the two types of HIV vary. The Type 1 is the most
common HIV worldwide; it is responsible for over 80% of the
global epidemic. The Subtype C of Group M is the most
prevalent. It is responsible for over a quarter of the global in
fection. It is followed by subtype B of the same group; it
is found in the industrialized countries of Western Europe and
North America, while infection with HIV-2 is less spread
and is confined mainly in West Africa. Additionally, the
HIV-2 AIDS progression is much slower and the virus is hardly
transmitted more easily because of its low infectivity and its
slow progress; especially as the Viral Loads (VL) in individuals
infected with HIV-2 are significantly lower.
Currently, no HIV-2 has been documented in Kinshasa or even
in the Democratic Republic of Congo (DRC). Hence, the objective
of this study was to determine the rate of HIV-1 and HIV-2
co-infection in Kinshasa population.
This study was a cross-sectional study on 115 randomly selected
plasma samples from the archived plasma samples of
newly infected individuals with HIV-1 without Antiretroviral
treatment collected between 2013 and 2014. 500µl of
plasma samples were stored at -20°C.140μl were used to extract RNA from plasma using the kit
QIAamp® RNA Mini Kit (QIAGEN, Hilden, Germany) in the Laboratory
of Molecular Biology to collect a final eluate of 60µl
[10]. For confirmation of the infection by HIV-1, a qualitative
real-time PCR, based on the previously referred test, was performed
on all 115 samples. Each sample (10µl) was analyzed
in duplicate.
A qualitative real-time PCR was conducted to determine the
HIV-2 infection according to the protocols described previously. Each sample (10µl) was also analyzed in duplicate.
In case of discrepancy between the PCR results, a 3rd Qualitative
Real Time PCR (a triplet) was performed.
All analysis were performed at Laboratory of Molecular Biology
of the Department of Basic Sciences of the Faculty of
Medicine of the University of Kinshasa.
113 samples of the 115 analyzed (98.3%) were positive for
HIV-1 using qualitative real-time PCR based on a previously
described test. Two samples which were previously positive, did not amplified even though the PCR tests used were
almost same. This difference can be caused by a conservation
problem or even thawing and freezing. Indeed, after freezing
and thawing, a sample loose close to 1.00 log10. This
means that samples which previously had low VL, i.e., less
than this threshold, should not be amplified after thawing
and freezing. This justifies the two samples that were not amplified
in the collection. These archived plasma samples were
previously used in other studies.Four samples out of 113 tested positive for HIV Type 2 by
qualitative real-time PCR giving HIV-1 and HIV-2 co-infectionrate of 4/113 or 3.54% for samples from a population of newly
infected patient’s naïve of treatment for HIV in Kinshasa. No
study to date has shown that coinfection in Kinshasa; these
results challenge the knowledge of the geographical distribution
of HIV-2.Our study uncovers the presentation of significant
AH in HIV infected individuals who were selected randomly.
Further research should be performed to look into
histopathological examination and study of the trends of CD4
counts associated with AH.
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