Pathology of HIV-1 Essay.
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Questions that these papers have raised for me:
Can CRV’s mutate as quickly as the HIV virus?
Can CRV’s keep up with the HIV viral mutations?
Will TIP therapy (specific CRV) be as effective in latter infection phases-versus initial infection phases?
Is it possible to pass TIP ‘therapy’ in the same manner HIV is passed? If so, will it also be effective in blocking infection in the new host?
Will TIP’s recognize all strains of HIV? Or will that require further genetic programming?
Since HIV-1 has an ‘army’ as it were, that down-regulates killer cell activating ligands within our immune system, how will TIP deal with that function?
Since we don;t fully understand how Nef and Vpu down-regulate the ligand PVR, how can we program CRV’s to identify and neutralize that function?
Conversely, might it be that if CRV’s can control HIV-1 infection, then the virus never gets to the point of down-regulating PVR ligand?
Here’s a snippet of the essay.
The first paper The Human Immunodeficiency Virus Type 1 NEF and VPU Proteins down regulate the Natural Killer Cell-Activating Ligand PVR by Matusali et al (2012) seeks to elucidate the mechanism through which the human immunodeficiency virus type – 1 (HIV-1) evades the immune actions of natural killer cells (NK cells). In this paper, the authors prove that the Nef protein down-modulates PVR (a ligand for DNAM-1 expressed in all NK cells) in HIV-1-infected T lymphocytes (Matusali et al, 2012).
The authors argue that the identified action of Nef proteins may be conserved by both patient-derived virus and laboratory HIV-1 strains but absent in HIV-2. Using laboratory methods, the authors report findings on the specific mechanisms through which HIV-1 downregulates PVR through the Nef protein. The results show that Nef protein downregulates HIV-1 through mechanisms; one of the mechanisms is altering the signal transduction pathways. The other mechanism is downregulating cell surface CD4, CXCR4, and human leucocyte antigen class 1. It is also reported that Nef protein can also inhibit the surface expression of HIV-1 infected cells as well as their recognition and lysis by HIV-specific T cells (CD8+). Through these activities, Nef protein is able to protect HIV- 1 infected cells from the immune system and facilitate the spread of the virus (Matusali et al, 2012).
In the second paper, Evolutionary Analysis of Human Immunodeficiency Virus Type 1 Therapy Based on Conditionally Replicating Vectors, Ke and Lloyd-Smith (2012) utilize the ‘therapeutic interfering particle’ as an example in analyzing a computational model of co-evolutionary dynamics of HIV-1 that act within-host and conditionally replicating vectors.
In the paper, the authors argue that efforts to reduce the viral load of HIV-1 have constantly been thwarted by the development of anti-viral resistant mutants. Ke and Lloyd (2012) also contend that although previous studies have revealed advantages of CRVs over anti-viral drugs, there is scanty research on evolutionary consequences of long-term CRV treatment. Therefore, the model discussed in this paper tracks the stochastic process of viral mutations deterministic population dynamics of T-cells and diverse strains of HIV-1 particles and Conditional Replicating Factors (CRV). The study reveals that during early co-infection, mutant HIV-1 genotypes that evade suppression by CRV therapies tend to appear. The authors further note that in HIV-1, the CRV population evolves to catch up with dominant escape mutant in HIV-1 and mostly persists in the long term.