Lung Bronchial Epithelial Cells are HIV Targets for Proviral Genomic Integration

Devadoss, Dinesh; Sp, Singh; Acharya, Arpan; Kc, Do; Periyasamy, Palsamy; Manevski, Marko; Mishra, Neerad C.; Tellez, Carmen S.; Ramakrishnan, Sundaram; Belinsky, Steven A.; Byrareddy, Siddappa N.; Buch, Shilpa; Chand, Hitendra S.; Sopori, Mohan L.

doi:10.1101/2020.06.01.126821

Cited by 4 publications

(4 citation statements)

References 48 publications

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“…These are not necessarily the epithelial cells of placenta. According to the recent preliminary report published in bioRxiv, HIV-1 can infect human bronchial epithelial cells; after exposition to HIV-1 they were shown to express p24 and contain latent HIV-1 provirus [ 85 ]. These findings along with the data by Asin SN et al [ 79 ] indicate that in certain cases epithelial cells can be infected with HIV-1, possibly as a one-round abortive infection with reverse transcription of RNA and integration of the proviral DNA governed by respective enzymes constituting HIV-1 virion.…”

Section: Mechanisms Underlying Hiv-1 Pathogenicity In Epithelial Cmentioning

confidence: 99%

Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

Isaguliants

Bayurova

Avdoshina

et al. 2021

Cancers

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People living with human immunodeficiency virus (HIV-1) are at increased risk of developing cancer, such as Kaposi sarcoma (KS), non-Hodgkin lymphoma (NHL), cervical cancer, and other cancers associated with chronic viral infections. Traditionally, this is linked to HIV-1-induced immune suppression with depletion of CD4+ T-helper cells, exhaustion of lymphopoiesis and lymphocyte dysfunction. However, the long-term successful implementation of antiretroviral therapy (ART) with an early start did not preclude the oncological complications, implying that HIV-1 and its antigens are directly involved in carcinogenesis and may exert their effects on the background of restored immune system even when present at extremely low levels. Experimental data indicate that HIV-1 virions and single viral antigens can enter a wide variety of cells, including epithelial. This review is focused on the effects of five viral proteins: envelope protein gp120, accessory protein negative factor Nef, matrix protein p17, transactivator of transcription Tat and reverse transcriptase RT. Gp120, Nef, p17, Tat, and RT cause oxidative stress, can be released from HIV-1-infected cells and are oncogenic. All five are in a position to affect “innocent” bystander cells, specifically, to cause the propagation of (pre)existing malignant and malignant transformation of normal epithelial cells, giving grounds to the direct carcinogenic effects of HIV-1.

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Section: Mechanisms Underlying Hiv-1 Pathogenicity In Epithelial Cmentioning

confidence: 99%

Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

Isaguliants

Bayurova

Avdoshina

et al. 2021

Cancers

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“…Replication persists in these reservoirs despite suppressive cART [72,73]. The lungs are anatomical reservoirs of HIV [74][75][76], with alveolar macrophages, intrapulmonary lymphocytes [75,76], and even bronchial epithelial cells serving as reservoirs [22,[77][78][79][80]. Several studies have reported that HIV can cause lung damage and inflammation that may contribute to the development of COPD.…”

Section: Pathogenesis Of Hiv and Circadian Disruptionmentioning

confidence: 99%

Circadian-Coupled Genes Expression and Regulation in HIV-Associated Chronic Obstructive Pulmonary Disease (COPD) and Lung Comorbidities

Panda

Chinnapaiyan

Rahman

et al. 2023

IJMS

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People living with HIV (PLWH) have an elevated risk of chronic obstructive pulmonary disease (COPD) and are at a higher risk of asthma and worse outcomes. Even though the combination of antiretroviral therapy (cART) has significantly improved the life expectancy of HIV-infected patients, it still shows a higher incidence of COPD in patients as young as 40 years old. Circadian rhythms are endogenous 24 h oscillations that regulate physiological processes, including immune responses. Additionally, they play a significant role in health and diseases by regulating viral replication and its corresponding immune responses. Circadian genes play an essential role in lung pathology, especially in PLWH. The dysregulation of core clock and clock output genes plays an important role in chronic inflammation and aberrant peripheral circadian rhythmicity, particularly in PLWH. In this review, we explained the mechanism underlying circadian clock dysregulation in HIV and its effects on the development and progression of COPD. Furthermore, we discussed potential therapeutic approaches to reset the peripheral molecular clocks and mitigate airway inflammation.

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“…Massive CD4 T-cell apoptosis during the acute infection phase is accompanied by profound immune activation, caused by release of apoptotic microparticles into the bloodstream ( 1 , 60 ). Furthermore, in addition to the attack on human immune cells, HIV also compromises the integrity of the lung epithelial barrier by infecting human bronchial epithelial cells, decreasing their expression of E-cadherin, and increasing paracellular permeability ( 61 , 62 ).…”

Section: Pulmonary Immune Dysregulation During Hiv Infectionmentioning

confidence: 99%

Pulmonary Immune Dysregulation and Viral Persistence During HIV Infection

2022

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Despite the success of antiretroviral therapy (ART), people living with HIV continue to suffer from high burdens of respiratory infections, lung cancers and chronic lung disease at a higher rate than the general population. The lung mucosa, a previously neglected HIV reservoir site, is of particular importance in this phenomenon. Because ART does not eliminate the virus, residual levels of HIV that remain in deep tissues lead to chronic immune activation and pulmonary inflammatory pathologies. In turn, continuous pulmonary and systemic inflammation cause immune cell exhaustion and pulmonary immune dysregulation, creating a pro-inflammatory environment ideal for HIV reservoir persistence. Moreover, smoking, gut and lung dysbiosis and co-infections further fuel the vicious cycle of residual viral replication which, in turn, contributes to inflammation and immune cell proliferation, further maintaining the HIV reservoir. Herein, we discuss the recent evidence supporting the notion that the lungs serve as an HIV viral reservoir. We will explore how smoking, changes in the microbiome, and common co-infections seen in PLWH contribute to HIV persistence, pulmonary immune dysregulation, and high rates of infectious and non-infectious lung disease among these individuals.

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Lung Bronchial Epithelial Cells are HIV Targets for Proviral Genomic Integration

Cited by 4 publications

References 48 publications

Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

Circadian-Coupled Genes Expression and Regulation in HIV-Associated Chronic Obstructive Pulmonary Disease (COPD) and Lung Comorbidities

Pulmonary Immune Dysregulation and Viral Persistence During HIV Infection

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