There is great concern about the impact of COVID-19 among the nearly 40 million people living with HIV (PLWH) worldwide. In this review, we surveyed current literature and found no evidence of higher prevalence of COVID-19 among PLWH but equivocal data on increased mortality and worse clinical outcomes. Having HIV does not confer protection against severe manifestations of COVID-19. Several studies looking at antiretroviral drugs against HIV to treat SARS-CoV-2 have shown no mortality benefit. Thus, there is no indication to change antiretroviral therapy (ART) regimens among virologically suppressed PLWH to prevent COVID-19. HIV care delivery has been adversely impacted in several countries during this pandemic but has created an opportunity for accelerating effective strategies like multi-month ART. Decentralizing HIV care in low-resource settings and incorporating telemedicine in high-resource settings will be critical in mitigating shocks to healthcare systems in the future.

J Biol Chem. 2006 Mar 31;281(13):8305-7. Epub 2005 Dec 30.

Viral agents of infectious disease such as human immunodeficiency virus (HIV),2 influenza virus, and hepatitis C virus (HCV) continue to pose daunting public health challenges. Substantial information is known about the multiplication cycles, the means of transmission, and the diseases caused by these three viruses, all of which are human pathogens that possess RNA genomes (1). Efforts to understand their viral multiplication schemes at the molecular level and to elucidate the interactions that occur between viral and cellular gene products that together determine the host’s susceptibility to infection and disease have led to significant new insights about HIV, influenza, and HCV viruses. The first two minireviews in this three-part series concern HIV and influenza virus. They focus on the genetic and biochemical aspects of two viral proteins, the Vif protein of HIV (2) and the M2 protein of influenza virus (3), and the functional roles that they play during establishment of productive viral infections. The third minireview focuses on the structure and function of the viral proteins involved in the replication of HCV RNA (4).

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Overview

In this new consolidated guidelines document on HIV prevention, diagnosis, treatment and care for key populations, the World Health Organization brings together all existing guidance relevant to five key populations – men who have sex with men, people who inject drugs, people in prisons and other closed settings, sex workers and transgender people – and updates selected guidance and recommendations.

These guidelines aim to:

provide a comprehensive package of evidence-based HIV-related recommendations for all key populations;
increase awareness of the needs of and issues important to key populations;
improve access, coverage and uptake of effective and acceptable services; and
catalyze greater national and global commitment to adequate funding and services.

Web annexes

The web annexes include the systematic reviews, literature review, values and preferences, supplementary case studies and technical briefs on HIV and young key populations that informed the development of guidance and recommendations for the Consolidated guidelines on HIV prevention, diagnosis, treatment and care for key populations.

Annex 1. Pre-exposure prophylaxis for men who have sex with men: a systematic review

Annex 2. Pre-exposure prophylaxis for people who inject drugs: a systematic review

Annex 3. Values and preferences: consolidated report

Annex 3.1 Values and Preferences of MSM: the use of antiretroviral therapy as prevention

Annex 3.2 Values and preferences of people who inject drugs, and views of experts, activists and service providers: HIV prevention, harm reduction and related issues

Annex 3.3 Values and preferences of transgender people: a qualitative study

Annex 4 Health interventions in prisons: a literature review

Annex 6.1 HIV and young transgender people

Annex 6.2 HIV and young people who sell sex

Annex 6.3 HIV and young people who inject drugs

Annex 6.4 HIV and young men who have sex with men

Ankara Ecz. Fak. Derg. 38 (1) 47- 78, 2009

HIV’in neden olduğu AIDS, ilk kez 1981 yılında ABD’de görülen bir enfeksiyon hastalığıdır. O zamandan beri AIDS hastalarının sayısı sürekli artmıştır. Aralık 2008 verilerine göre dünyada 33.4 milyon kişi HIV virüsü ile yaşamaktadır. HIV’in özelliklerinin belirlenmesi ile birlikte anti-HIV ilaçlar klinik kullanıma girmeye başlamıştır. Farklı etki mekanizmalarına sahip ilaçlar AIDS tedavisinde kullanılmaya başlamış ve yedi ilaç grubundan oluşan Highly Active Anti-Retroviral Therapy (HAART) 1996 yılında ortaya çıkmıştır. Bugün HAART HIV’e karşı standart tedavidir. HAART’ın kullanımı ilaçların toksik yan etkilerinde ve HIV’in çoğalmasında önemli bir azalmaya neden olmuştur. Böylece AIDS nedeniyle ölen insan sayısı azalmıştır. Bütün bu olumlu gelişmelere rağmen, çalışmalar, HIV’i eradike edecek ve AIDS tedavisinde kullanılacak yeni anti-HIV ajanların keşfini sağlamak amacıyla devam etmektedir.

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ISBN 978-953-307-442-9, Hard cover, 364 pages
Publisher: InTech
Publication date: November 2011
Subject: Infectious Diseases

HIV remains the major global health threat, and neither vaccine nor cure is available. Increasing our knowledge on HIV infection will help overcome the challenge of HIV/AIDS. This book covers several aspects of HIV-host interactions in vitro and in vivo. The first section covers the interaction between cellular components and HIV proteins, Integrase, Tat, and Nef. It also discusses the clinical relevance of HIV superinfection. The next two chapters focus on the role of innate immunity including dendritic cells and defensins in HIV infection followed by the section on the impact of host factors on HIV pathogenesis. The section of co-infection includes the impact of Human herpesvirus 6 and Trichomonas vaginalis on HIV infection. The final section focuses on generation of HIV molecular clones that can be used in macaques and the potential use of cotton rats for HIV studies.

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ISBN 978-953-307-871-7, Hard cover, 132 pages
Publisher: InTech
Publication date: January 2012
Subject: Infectious Diseases

It can be said that now is the best time for everyone infected to become aware of their own HIV status. The state of the art in HIV management progressively reveals that antiretroviral treatment can prevent transmission, as well as chronic damage in the human body, if started early. Unfortunately, antiretrovirals are not widely available in many places, especially in developing countries. In these parts of the world, diagnosis of HIV infection must be kept in the agenda as a priority, in order to understand specific details of local epidemics and as an effort to interrupt the chain of HIV transmission.

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Retrovirology. 2011 Jul 1;8:52.
Abstract

Integration of the reverse transcribed viral genome into host chromatin is the hallmark of retroviral replication. Yet, during natural HIV infection, various unintegrated viral DNA forms exist in abundance. Though linear viral cDNA is the precursor to an integrated provirus, increasing evidence suggests that transcription and translation of unintegrated DNAs prior to integration may aid productive infection through the expression of early viral genes. Additionally, unintegrated DNA has the capacity to result in preintegration latency, or to be rescued and yield productive infection and so unintegrated DNA, in some circumstances, may be considered to be a viral reservoir. Recently, there has been interest in further defining the role and function of unintegrated viral DNAs, in part because the use of anti-HIV integrase inhibitors leads to an abundance of unintegrated DNA, but also because of the potential use of non-integrating lentiviral vectors in gene therapy and vaccines. There is now increased understanding that unintegrated viral DNA can either arise from, or be degraded through, interactions with host DNA repair enzymes that may represent a form of host antiviral defence. This review focuses on the role of unintegrated DNA in HIV infection and additionally considers the potential implications for antiviral therapy.

The various forms of unintegrated HIV cDNA. Linear cDNA, the product of reverse transcription, is susceptible to a number of fates other than integration into host chromatin as proviral DNA. Autointegration may lead to the formation of truncated or internally rearranged circular forms. Although recombination may yield 1-LTR circles, host factors may also contribute their presence. Host factors, such as those involved in the non-homologous end joining pathway, participate in the formation of 2-LTR circles. Various DNA repair factors and restriction factors may also result in direct degradation of linear cDNA. Collectively, these processes help to explain patterns of unintegrated viral DNA present in infected cells.

Transcription from preintegrated or unintegrated DNA. Prior to integration, or if integration is blocked, transcription from unintegrated cDNA may still occur, the template for which is unknown. Virally imported Vpr is important in the initial stages of viral gene transcription. Translation of multiply-spliced RNA (msRNA) transcripts leads to expression of Tat, Nef and Rev. Levels of Rev are insufficient to lead to the export of singly spliced and unspliced transcripts. Rev is thought to later interfere with the integration process and to thereby inhibit superinfection. Tat and Nef collectively lead to increased cellular activation in resting T-cells. Newly synthesized Tat will also promote viral gene transcription. Nef downregulates cell surface CD4, CXCR4, CCR5 and MHC-I (HLA Class I), thereby limiting superinfection, signal transduction and likely resulting evasion from cytotoxic T-lymphocytes. Preintegration transcription of viral genes has also been linked to altered cytokine secretion in both resting T-cells and macrophages.

Top HIV Med. 2009 Dec;17(5):138-45.

This December 2009 version of the International AIDS Society–USA (IAS–USA) drug resistance mutations list updates the figures last published in December 2008 (Johnson VA et al, Top HIV Med, 2008;16:138-145). This update includes 3 new mutations—K65R for stavudine (Hawkins CA et al, JAIDS, 2009;52:228- 234 and Wallis C et al, JAIDS, October 2009; Epub ahead of print) and K101P for efavirenz and nevirapine (Parkin NT et al, Antimicrob Agents Chemother, 2006;50:351-354; Rhee SY et al, Antimicrob Agents Chemother, 2004:48:3122-3126; and Rhee SY et al, Proc Natl Acad Sci USA, 2006;46:17355-17360). In addition, the darunavir I47V mutation and the lopinavir/ritonavir L76V mutation designations were changed to boldface to indicate their recognition as major rather than minor mutations. One mutation, L33F for tipranavir/ritonavir, was changed from a major mutation to that of a minor to reflect recent information.
Also, many of the user notes were substantially revised.