HIV: ART and Immune Activation

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (15 June 2019) | Viewed by 9324

Special Issue Editors


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Guest Editor
Department of Pharmacology and Experimental Neuroscience, College of Medicine, University of Nebraska Medical Center, Omaha, NE, USA
Interests: HIV-1; inflammation; animal models; neuroAIDS; adjunctive therapeutics

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Guest Editor
Department of Pharmacology, University of Nebraska Medical Center, Omaha, NE, USA
Interests: HIV-1 pathogenesis; animal models; viral hepatitis B and C; drug testing

Special Issue Information

Dear Colleagues,

Antiretroviral therapy (ART) has greatly reduced HIV infection-associated morbidity and mortality. ART improved the lifespan of persons living with HIV infection by reducing viral replication, restoring CD4+ T cells and preventing the progression of HIV infection to acquired immunodeficiency syndrome (AIDS). However, despite long-term ART, low level of viral replication persists in HIV reservoirs residing in resting CD4+ T cells in the blood, central nervous system (CNS), gut-associated lymphoid tissue, bone marrow, and genital tract. Persisting low level viral replication in the ART controlled patients can contribute to sustained systemic immune activation and inflammation. ART reduces systemic inflammation and immune activation dramatically, but not to levels synchronous with HIV-uninfected populations. HIV proteins such as gp120 and Tat, secreted from HIV reservoirs, are capable of inducing generation of reactive oxygen species (ROS) which in turn can initiate immune activation/inflammation via production of cytokines and chemokines. Chronic inflammation has the potential to attenuate the efficacy of ART as well as promote pathological conditions and end-organ disease in HIV patients. Indeed in HIV patients on long-term ART, inflammation has been linked to cardiovascular disease (CVD), neurocognitive dysfunction, osteoporosis, cancer, muscle wasting, premature aging and frailty among others. 

In this special issue we will focus on molecular mechanisms underlying persisting immune activation and inflammation in ART suppressed HIV infected patients, and also that are affecting various end-organ functions. Such comprehensive issue will deliver an overall understanding on the effect of inflammation on HIV and ART related diseases, and provide prospect for the development of therapeutics.   

Assoc. Prof. Santhi Gorantla
Prof. Larisa Poluektova
Guest Editors

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Keywords

  • HIV-1 pathogenesis
  • ART
  • Inflammation
  • Immune activation
  • Cardiovascular diseases
  • Liver diseases
  • Neuroinflammation
  • Renal diseases
  • Obesity
  • Muscle wasting
  • Premature aging

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Published Papers (1 paper)

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Review

18 pages, 21619 KiB  
Review
HIV Vaccine Mystery and Viral Shell Disorder
by Gerard Kian-Meng Goh, A. Keith Dunker, James A. Foster and Vladimir N. Uversky
Biomolecules 2019, 9(5), 178; https://doi.org/10.3390/biom9050178 - 8 May 2019
Cited by 41 | Viewed by 8481
Abstract
Hundreds of billions of dollars have been spent for over three decades in the search for an effective human immunodeficiency virus (HIV) vaccine with no success. There are also at least two other sexually transmitted viruses, for which no vaccine is available, the [...] Read more.
Hundreds of billions of dollars have been spent for over three decades in the search for an effective human immunodeficiency virus (HIV) vaccine with no success. There are also at least two other sexually transmitted viruses, for which no vaccine is available, the herpes simplex virus (HSV) and the hepatitis C virus (HCV). Traditional textbook explanatory paradigm of rapid mutation of retroviruses cannot adequately address the unavailability of vaccine for many sexually transmissible viruses, since HSV and HCV are DNA and non-retroviral RNA viruses, respectively, whereas effective vaccine for the horsefly-transmitted retroviral cousin of HIV, equine infectious anemia virus (EIAV), was found in 1973. We reported earlier the highly disordered nature of proteins in outer shells of the HIV, HCV, and HSV. Such levels of disorder are completely absent among the classical viruses, such as smallpox, rabies, yellow fever, and polio viruses, for which efficient vaccines were discovered. This review analyzes the physiology and shell disorder of the various related and non-related viruses to argue that EIAV and the classical viruses need harder shells to survive during harsher conditions of non-sexual transmissions, thus making them vulnerable to antibody detection and neutralization. In contrast, the outer shell of the HIV-1 (with its preferential sexual transmission) is highly disordered, thereby allowing large scale motions of its surface glycoproteins and making it difficult for antibodies to bind to them. The theoretical underpinning of this concept is retrospectively traced to a classical 1920s experiment by the legendary scientist, Oswald Avery. This concept of viral shapeshifting has implications for improved treatment of cancer and infections via immune evasion. Full article
(This article belongs to the Special Issue HIV: ART and Immune Activation)
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