BSCI 2201L Lecture Notes - Lecture 99: Antiviral Drug, Polyadenylation, Hepatitis C Virus
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Prof. Jason Pitts
Review Paper Proposal
This paper review report is intended to explore the molecular mechanisms of HIV
pathogenesis. Since the HIV/AIDS epidemic exploded around the end of the last century, a lot of
research effort has been going to finding a vaccine for HIV and developing antiviral drugs that
prevent the virus from hijacking cell machinery. This requires understanding how the virus
works in the cell in order to develop effective ways for intervening in the virus pathogenic
In this paper, I will start with exploring articles about HIV pathogenesis in general. I will
attempt to understand two things: How does the virus interact with the host cell, and how can it
evade innate immune responses. Then I want to shift my attention to intrinsic methods that the
cell uses to evade the effects of HIV and dismantle the viral capsid before it replicates. It has
been shown that individuals who are HLA-B27 positive are more likely to remain symptom-free
for years after HIV infection. I will explore the role that HLA-B27 plays in the process of HIV
The last part of this paper will zoom in on cleavage and polyadenylation specificity factor
subunit 6 CPSF6. This subunit is involved in the mRNA maturation process. However, it has
been shown that it interacts with the viral capsid at specific sites that affect the process of
transfection. I will review papers that address the molecular function of CPSF6 and the structure
site of capsid that is targeted by CPSF6.
My overall goal of this exercise is to learn how to extract important information out of
scientific papers and compile them to gain a systematic understanding of HIV and its molecular
interactions that may be the basis for an HIV antiviral drug or preventive vaccine.
Virus-host interactions in HIV pathogenesis: directions for therapy.
HIV-1 evades innate immune recognition through specific cofactor recruitment.
Progression of HIV to AIDS: a protective role for HLA-B27?
[Protective role of HLA-B27 in HIV and hepatitis C virus infection]
Pressure from TRIM5α contributes to control of HIV-1 replication by individuals expressing
protective HLA-B alleles.