Mechanisms underlying of antiretroviral drugs in different cellular reservoirs with a focus on macrophages

Aquaro, Stefano; Borrajo, Ana; Pellegrino, Michele; Svicher, Valentina

doi:10.1080/21505594.2020.1760443

Cited by 21 publications

(17 citation statements)

References 120 publications

(157 reference statements)

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“… 35 The viral capsid also houses enzymes essential for viral replication, eg, reverse transcriptase, integrase and proteases, coded by the viral pol gene. 36 The viral reverse transcriptase converts the HIV RNA into DNA when the virus enters the host. 37 , 38 Integrase can then incorporate the viral DNA into the host DNA, creating a permanent copy of the viral DNA in the cell.…”

Section: Key Components: Armamentsmentioning

confidence: 99%

SARS-CoV-2 and Human Immunodeficiency Virus: Pathogen Pincer Attack

Evans¹,

Martínez²,

Petrosillo³

et al. 2021

HIV

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Paramount efforts worldwide are seeking to increase understanding of the basic virology of SARS-CoV-2, characterize the spectrum of complications associated with COVID-19, and develop vaccines that can protect from new and recurrent infections with SARS-CoV-2. While we continue learning about this new virus, it is clear that 1) the virus is spread via the respiratory route, primarily by droplets and contact with contaminated surfaces and fomites, as well as by aerosol formation during invasive respiratory procedures; 2) the airborne route is still controversial; and 3) that those infected can spread the virus without necessarily developing asymptomatic). With the number of SARS-CoV-2 infections increasing globally, the possibility of co-infections and/or co-morbidities is becoming more concerning. Co-infection with Human Immunodeficiency Virus (HIV) is one such example of polyparasitism of interest. This military-themed comparative review of SARS-CoV-2 and HIV details their virology and describes them figuratively as separate enemy armies. HIV, an old enemy dug into trenches in individuals already infected, and SARS-CoV-2 the new army, attempting to attack and capture territories, tissues and organs, in order to provide resources for their expansion. This analogy serves to aid in discussion of three main areas of focus and draw attention to how these viruses may cooperate to gain the upper hand in securing a host. Here we compare their target, the key receptors found on those tissues, viral lifecycles and tactics for immune response surveillance. The last focus is on the immune response to infection, addressing similarities in cytokines released. While the majority of HIV cases can be successfully managed with antiretroviral therapy nowadays, treatments for SARS-CoV-2 are still undergoing research given the novelty of this army.

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Section: Key Components: Armamentsmentioning

confidence: 99%

SARS-CoV-2 and Human Immunodeficiency Virus: Pathogen Pincer Attack

Evans¹,

Martínez²,

Petrosillo³

et al. 2021

HIV

View full text Add to dashboard Cite

show abstract

“…Productive HIV infection occurs in perivascular macrophages, MDMs, and microglia [34]. While it is sufficiently established that neuronal injury and loss are correlated with the evolution of HAND manifestations, there is a paucity of available information on the capability of HIV to infect neurons [13,35]. In accordance with the broadly accepted model, in a systemic infection, after at least 1 week, the virus enters the CNS through the BBB, infecting it via a "Trojan horse" pattern [36] (Figure 1).…”

Section: Pathology Of Neuroaidsmentioning

confidence: 99%

“…Within the CNS, the virus does not infect neuronal cells; it can establish an infection in different types of cells [13]. Perivascular macrophages, microglial cells, and possibly astrocytic cells produce viral proteins that cause inflammation and, in turn, lead to HIV-1induced neuronal damage [14].…”

Section: Introductionmentioning

confidence: 99%

Crucial Role of Central Nervous System as a Viral Anatomical Compartment for HIV-1 Infection

et al. 2021

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The chronic infection established by the human immunodeficiency virus 1 (HIV-1) produces serious CD4+ T cell immunodeficiency despite the decrease in HIV-1 ribonucleic acid (RNA) levels and the raised life expectancy of people living with HIV-1 (PLWH) through treatment with combined antiretroviral therapies (cART). HIV-1 enters the central nervous system (CNS), where perivascular macrophages and microglia are infected. Serious neurodegenerative symptoms related to HIV-associated neurocognitive disorders (HAND) are produced by infection of the CNS. Despite advances in the treatment of this infection, HAND significantly contribute to morbidity and mortality globally. The pathogenesis and the role of inflammation in HAND are still incompletely understood. Principally, growing evidence shows that the CNS is an anatomical reservoir for viral infection and replication, and that its compartmentalization can trigger the evolution of neurological damage and thus make virus eradication more difficult. In this review, important concepts for understanding HAND and neuropathogenesis as well as the viral proteins involved in the CNS as an anatomical reservoir for HIV infection are discussed. In addition, an overview of the recent advancements towards therapeutic strategies for the treatment of HAND is presented. Further neurological research is needed to address neurodegenerative difficulties in people living with HIV, specifically regarding CNS viral reservoirs and their effects on eradication.

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“…Macrophages or microglia can provoke the release of pr-inflammatory cytokines, including tumor necrosis factor α (TNFα), interferon α (IFNα), interleukin-6 (IL6), interleukin-8 (IL8), and interleukin-1β (IL1β) [ 6 , 8 , 13 ] ( Figure 1 ), as well as chemokines (C-C motif chemokine ligand 2 (CCL2) and C-C motif chemokine ligand 5 (CCL5), macrophage inflammatory protein 1β (MIP)-1β) [ 17 ]. These clues indicate the existence of cellular reservoirs in the CNS established within 3 to 5 days of HIV-1 infection [ 8 ], comprising three different types of long-lived infected cells [ 18 ]: astrocytes, monocyte lineage cells [ 19 ], and microglial cells [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Microglia: The Real Foe in HIV-1-Associated Neurocognitive Disorders?

et al. 2021

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The current use of combined antiretroviral therapy (cART) is leading to a significant decrease in deaths and comorbidities associated with human immunodeficiency virus type 1 (HIV-1) infection. Nonetheless, none of these therapies can extinguish the virus from the long-lived cellular reservoir, including microglia, thereby representing an important obstacle to curing HIV. Microglia are the foremost cells infected by HIV-1 in the central nervous system (CNS) and are believed to be involved in the development of HIV-1-associated neurocognitive disorder (HAND). At present, the pathological mechanisms contributing to HAND remain unclear, but evidence suggests that removing these infected cells from the brain, as well as obtaining a better understanding of the specific molecular mechanisms of HIV-1 latency in these cells, should help in the design of new strategies to prevent HAND and achieve a cure for these diseases. The goal of this review was to study the current state of knowledge of the neuropathology and research models of HAND containing virus susceptible target cells (microglial cells) and potential pharmacological treatment approaches under investigation.

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Mechanisms underlying of antiretroviral drugs in different cellular reservoirs with a focus on macrophages

Cited by 21 publications

References 120 publications

SARS-CoV-2 and Human Immunodeficiency Virus: Pathogen Pincer Attack

SARS-CoV-2 and Human Immunodeficiency Virus: Pathogen Pincer Attack

Crucial Role of Central Nervous System as a Viral Anatomical Compartment for HIV-1 Infection

Microglia: The Real Foe in HIV-1-Associated Neurocognitive Disorders?

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