Pathogenesis of HIV-1 infection – chosen aspects

Knysz, Brygida; Szetela, Bartosz; Gładysz, Andrzej

doi:10.1016/s1730-1270(10)60035-5

Cited by 5 publications

(4 citation statements)

References 32 publications

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“…It comprises 15 proteins and two copies of positive strand genomic RNA . Upon entry HIV‐1 genome is reverse transcribed, and the resulting double‐strand DNA is integrated within the host genome through complex mechanisms involving both viral and cellular proteins . HIV‐1 infects CD4+ cells such as T helper lymphocytes, macrophages, dendritic cells and brain‐resident microglia .…”

Section: Hiv‐1‐encoded Mirnas a Controversial Findingmentioning

confidence: 99%

MicroRNAs, HIV and HCV: a complex relation towards pathology

Piedade

Azevedo‐Pereira

2016

Reviews in Medical Virology

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MicroRNAs are small non-coding RNAs that modulate protein production by post-transcriptional gene regulation. They impose gene expression control by interfering with mRNA translation and stability in cell cytoplasm through a mechanism involving specific binding to mRNA based on base pair complementarity. Because of their intracellular replication cycle it is no surprise that viruses evolved in a way that allows them to use microRNAs to infect, replicate and persist in host cells. Several ways of interference between virus and host-cell microRNA machinery have been described. Most of the time, viruses drastically alter host-cell microRNA expression or synthesize their own microRNA to facilitate infection and pathogenesis. HIV and HCV are two prominent examples of this complex interplay revealing how fine-tuning of microRNA expression is crucial for controlling key host pathways that allow viral infection and replication, immune escape and persistence. In this review we delve into the mechanisms underlying cellular and viral-encoded microRNA functions in the context of HIV and HCV infections. We focus on which microRNAs are differently expressed and deregulated upon viral infection and how these alterations dictate the fate of virus and cell. Copyright © 2016 John Wiley & Sons, Ltd.

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Section: Hiv‐1‐encoded Mirnas a Controversial Findingmentioning

confidence: 99%

MicroRNAs, HIV and HCV: a complex relation towards pathology

Piedade

Azevedo‐Pereira

2016

Reviews in Medical Virology

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“…There tends to be an increase in nuclear transcription factor and inflammatory cytokine activation of the immune system (Brach et al;1992). The progression of the virus/infection will then allow for opportunistic infections which then would also promote more oxidative stress due to increased free radical elements, again improving viral replication and weakening antioxidant defense (Knysz, 2007). Damage or altering of the DNA repair machinery is an important aspect of the progression of HIV infection pathogenesis (Olinski et al;.…”

Section: Hiv and Free Radicalsmentioning

confidence: 99%

Role of Cytokines and Chemokines in HIV Infection

Venketaraman¹,

Morris²,

Donohou³

et al. 2011

HIV and AIDS - Updates on Biology, Immunology, Epidemiology and Treatment Strategies

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“…Both Françoise Barré-Sinoussi and Luc Montagnier shared the Nobel Prize in 2008 in Medicine or Physiology for their discovery of HIV [3][4][5]. The basis for this award was that they discovered the HIV and also demonstrated that the virus is produced in the lymphocytes of patients with enlarged lymph nodes at early stages of immune deficiency and in the blood of patients at advanced stages of the disease, that helped to build up the current understanding of the biology of this disease and of the antiretroviral therapy [6][7][8][9][10]. Since its first discovery in 1981, HIV/AIDS has killed more than 25 million people worldwide and is today the major threat to human health.…”

Section: Introductionmentioning

confidence: 99%

Cell cycle checkpoints and pathogenesis of HIV-1 infection: a brief overview

Kurapati

Samikkannu

Atluri

et al. 2014

Journal of Basic and Clinical Physiology and Pharmacology

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To understand HIV pathogenesis or development is no simple undertaking and neither is the cell cycle which is highly complex that requires the coordination of multiple events and machinery. It is interesting that these two processes are interrelated, intersect and interact as HIV-1 infection results in cell cycle arrest at the G2 phase which is accompanied by massive CD4+ T cell death. For its own benefit, in an impressive manner and with the overabundance of tactics, HIV maneuvers DNA damage responses and cell cycle check points for viral replication at different stages from infection, to latency and to pathogenesis. Although the cell cycle is the most critical aspect involved in both viral and cellular replication, in this review, our main focus is on recent developments, including our own observations in the field of cell cycle proteins, checkpoints and strategies utilized by the viruses to manipulate these pathways to promote their own replication and survival. We will also discuss the emerging concept of targeting the replication initiation machinery for HIV therapy.

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Pathogenesis of HIV-1 infection – chosen aspects

Cited by 5 publications

References 32 publications

MicroRNAs, HIV and HCV: a complex relation towards pathology

MicroRNAs, HIV and HCV: a complex relation towards pathology

Role of Cytokines and Chemokines in HIV Infection

Cell cycle checkpoints and pathogenesis of HIV-1 infection: a brief overview

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