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HIV/AIDS
Published in Patricia G. Melloy, Viruses and Society, 2023
HIV is a retrovirus. Humans are born with what are known as “endogenous retroviruses” in their genome, in addition to possibly acquiring “exogenous retroviruses” like human T-cell leukemia virus (HTLV) and HIV during their lifetimes. Endogenous retroviruses include fragments or whole retroviruses that embedded in our DNA during human evolution and rarely cause disease (Cloyd 1996). HIV is in the Lentivirus genus, a type of enveloped retrovirus that uses reverse transcriptase to make a DNA copy of its genome that then inserts into the host cell genome (Zimmer 2011; Lostroh 2019; Cloyd 1996). Lentiviruses are known for causing chronic infections with a long incubation period, primarily attacking the immune system or the nervous system (Tang, Kuhen, and Wong-Staal 1999; Cruse and Lewis 2009). Lentiviruses are of the Baltimore classification Class VI, which is a single-stranded RNA virus that uses a DNA intermediate for replication (Baltimore 1971). Lentiviruses possess the three critical genes found in any retrovirus: gag, pol, and env, which are necessary for making the structural proteins and enzymes required by the virus (Tang, Kuhen, and Wong-Staal 1999).
Endogenous Proviruses
Published in Pimentel Enrique, Oncogenes, 2020
The possible role of endogenous retroviruses in malignant diseases is not understood. Virions morphologically identical to type-C retroviruses appear at low frequency in human tumor cells, including embryonal carcinoma cell lines established from human testicular tumors and teratocarcinoma cell lines.26,27
Mobile DNA Sequences and Their Possible Role in Evolution
Published in S. K. Dutta, DNA Systematics, 2019
Georgii P. Georgiev, Yurii V. Ilyin, Alexei P. Ryskov, Tatiana I. Gerasimova
In European strains of mice the IAP genes are very numerous (800 to 1000 copies). The Asiatic mice contain fewer copies of this mdg-like element (only 25 to 50 copies).84 Different endogenous retroviruses are detected in chicken, mice, and monkeys. Many of them reveal considerable sequence homology. Some homology can even be detected between mdg elements of D. melanogaster 297 and 17.6 and the avian leukosis-sarcoma retrovirus (AL-SV).26
Allostatic Load, Mobility Disability, and Viral Effects in Cancer: A Structural Equation Model
Published in Cancer Investigation, 2022
Oncogenic RNA viruses include the Human Immunodeficiency Virus (HIV), Human T Lymphocyte Virus (HTLV-1), and Hepatitis C. With the RNA viruses, there is the capacity for the latent viruses to become activated epigenetically via environmental and physiological stressors to be expressed and trigger cellular transformations (36). Possibly 8-20 percent of the human genome consists of endogenous retroviruses (ERV) or retroelements (36). These ERV variants include Syncytin 1 and 2, both of which are essential for the highly fused placenta in humans and other eutherian mammals whereas other variants have been associated with cancerous cell fusions (37). Endogenous retroviruses represent a poorly understood yet significant component of the genome that may be involved in stress-related pathologies.
Enhanced expression of human endogenous retroviruses in new-onset type 1 diabetes: Potential pathogenetic and therapeutic implications
Published in Autoimmunity, 2020
Pier-Angelo Tovo, Ivana Rabbone, Davide Tinti, Ilaria Galliano, Michela Trada, Valentina Daprà, Franco Cerutti, Massimiliano Bergallo
Cocktails of antiretroviral drugs are used for years in HIV-positive subjects and their optimal doses and side effects are well-known. Some products can reduce the expression of endogenous retroviruses in vitro [43]. HERVs are particularly transactivated in HIV + individuals [44] and antiretroviral therapy reduces the viral load not only of HIV but also of HERVs [45,46]. Notably, HERV transcription is enhanced by inflammatory signals that through the ubiquitin-proteasome cascade activate NF-kB; following its passage into the nucleus this binds specific sequences of HERV proviruses triggering their transcription [47]. We demonstrated that antiretroviral drugs display an intrinsic anti-proteasome activity [48,49]. Consequently, these drugs can reduce HERV transcription not only through a direct specific action against retroviruses, but also through indirect effects on host cell components. Therefore, the administration of antiretroviral drugs in new-onset T1D appears an exciting speculation potentially heralding a new therapeutic strategy.
Retroviruses in the pathogenesis of systemic lupus erythematosus: Are they potential therapeutic targets?
Published in Autoimmunity, 2020
Rossella Talotta, Fabiola Atzeni, Magdalena Janina Laska
The family of Retroviridae encompasses exogenous retroviruses, horizontally transmitted through somatic cells, and endogenous retroviruses, vertically transmitted in germinal cells. Endogenous retroviruses are the remnants of ancient exogenous retroviral infections, integrated in host genome during human evolution. Genetic mutations accumulated over the time have altered their original sequence, thus preventing their complete life-cycle [44]. In humans, HERVs are traceable in about 8% of nuclear DNA [45], and are inherited in a Mendelian fashion as they take part to each individual’s genetic makeup. HERV sequences coding for gag, pol and env are flanked at the 5’untraslated regions (UTR) and 3’UTR by long terminal repeats (LTRs), generated by reverse transcriptase-dependent strand duplication. LTRs, often as solitary elements, are spread in many copies throughout the genome as the result of a high number of replication cycles. LTRs have regulatory domains and can contribute to the control in cis of adjacent gene transcription [46]. Due to defective open reading frames (ORFs), HERVs lost their infectivity and only few of them retain the capability of translating their proteins. It has been reported, on the contrary, that some LTRs have a still preserved regulatory activity (ranging from 10% to 38% according to the anatomical district) [47], and contain functional promoter and enhancer sequences [48]. Despite mainly working as alternative promoters and having a minor impact on gene transcription, LTRs are noteworthy active in germ line cells and placenta, where they may contribute to morphogenesis [47]. Therefore, the expression of LTRs seems tissue-specific and kept under control by epigenetics. Profound epigenetic modifications, occurring, for instance, in autoimmunity and cancer, may reset their activity and favour the transcription of LTR-dependent genes involved in the inflammatory response and carcinogenesis [49].