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What Are The Impacts Of Hiv Aids
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Hiv Stigma: Perspectives From Kenyan Child Caregivers And Adolescents Living With Hiv
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Google Scholar View edition*, Jianyu Liu Jianyu Liu Skill Printers.
Department of Pharmacology and Experimental Neuroscience, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198-5880, USA
Hiv/aids Impact In Africa
Received: 12 April 2023 / Revised: 1 May 2023 / Accepted: 2 May 2023 / Published: 5 May 2023
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the 2019 coronavirus disease (Covid-19) pandemic, a fatal respiratory disease. Risk factors associated with COVID-19 include older age and comorbidities In the combination antiretroviral therapy (cART) era, a significant proportion of people living with HIV (PLWH) with controlled viremia are older and have comorbidities, making these individuals more susceptible to SARS-CoV-2 infection and severe COVID-19. associated disease. RESULTS. In addition, SARS-CoV-2 has neurodegenerative effects and causes neurological complications that negatively impact the health burden and PLWH as well as HIV-associated neurodegenerative disease (NDD). Consequences of SARS-CoV. 2 infection and the severity of COVID-19 on neuroinflammation, HAND, and HAND development have not been fully explored before. In the present review, we examine the differences and similarities between SARS-CoV-2 and HIV-1, SARS. We have collected the current knowledge. -On CoV-2/Covid-19 syndrome and HIV-//AIDS. Central nervous system (CNS). Risk factors for PLWH and neurological manifestations of COVID-19, inflammatory mechanisms leading to neurological syndromes, development of HAND and its impact on its predecessor HAND are also discussed Finally, we consider the challenges of the current epidemic for the global population, with special emphasis on PLWH on
The world is in the midst of a debilitating coronavirus disease 2019 (Covid-19) pandemic, coinciding with the acquired immunodeficiency syndrome (AIDS) epidemic [1, 2, 3]. The causative agent of COVID-19 is severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), and in the case of AIDS, human immunodeficiency virus type 1 (HIV-1). [4, 5, 6, 7, 8]. Worldwide, the number of SARS-CoV-2 infections has exceeded 758 million, and more than 6.8 million have died due to COVID-19. However, a total of 84.2 million people became infected with HIV-1 and 40.1 million died of AIDS-related illnesses. In 2021, the number of people living with HIV-1 (PLWH) is 38.4 million, with 1.5 million new infections and more than 650,000 deaths [ 10 , 11 ]. Co-infection of SARS-CoV-2 and HIV-1 leads to simultaneous or SARS-CoV-2/Covid-19/and HIV-1/AIDS syndrome [12, 13]. PLWH are thought to be at risk of SARS-CoV-2 infection and their dysregulated immunity and inflammatory consequences, but there is no clear consensus [ 13 , 14 , 15 , 16 , 17 , 18 ]. The small increase in risk may be due to viral load suppression and quasi-immune recovery with antiretroviral therapy (cART) regimens. However, global reports have shown increased morbidity and mortality from SARS-CoV-2 infection in PLWH compared to HIV-1-infected individuals [ 19 , 20 , 21 , 22 , 23 ]. In addition to respiratory syndrome, COVID-19 also causes neurological manifestations such as headache, confusion, impaired consciousness, loss of smell, hearing loss, meningitis, neurological disease and other symptoms are different [24, 25, 26, 27]. Therefore, the frequency of neurological manifestations associated with COVID-19 is consistent with neurological manifestations in PLWH and HIV patients.
Entry of HIV-1 into the central nervous system (CNS) was discovered early in the HIV-1 epidemic, and brain infection has been thoroughly studied and characterized, as well as viral proteins and their neurotoxicity [ 30 , 31 , 32 ]. Emerging evidence suggests that SARS-CoV-2 enters the central nervous system and modulates host immune responses, leading to neurological manifestations [ 33 , 34 , 35 ]. Post-acute effects of SARS-CoV-2 (PASC) or chronic-covid have been shown to adversely affect PLWH, especially those with HAND [ 36 , 37 ]. This review describes recent developments in neurological manifestations caused by SARS-CoV-2/Covid-19 in PLWH with or without HAR. It covers the similarities and differences between SARS-CoV-2 and HIV-1 to describe the neurological manifestations caused by SARS-CoV-2 with classes of neurological effects caused by HIV-1; Risk factors for COVID-19 and neurological sequelae of SARS-CoV-2/Covid-19 and HIV-1/AIDS syndromes in PLWH. and explore potential mechanisms focusing on neurological sequelae and neurotoxicity associated with NLRP3 inflammasome overactivation in PLWH SARS-CoV-2 infection [ 38 , 39 ]. In addition, the challenges of COVID-19 for PLWH, the incidence of PASC and prolonged COVID, and potential ways to mitigate the overwhelming impact of SARS-CoV-2 syndrome/HIV-1 are discussed.
Botswana Hiv/aids Impact Survey Report
SARS-CoV-2 and HIV-1 are naturally occurring RNA viruses that infect humans through zoonotic transmission [ 40 , 41 ]. Despite their differences, these bacteria use common molecular mechanisms during infection and disease development [ 3 , 41 , 42 , 43 ]. Similarities between SARS-CoV-2/Covid-19 and HIV-1/AIDS are described below and summarized in Table 1. The differences are shown in Table 2
Public fear is a common feature of both SARS-CoV-2 and HIV-1 viral infections. This societal fear makes people mentally ill, leading to stress and anxiety
Both SARS-CoV-2 and HIV Furthermore, immunocompromised PLWH harbor SARS-CoV-2 for longer periods of time, allowing sufficient time for mutations to accumulate and lead to the emergence of SARS-CoV-2 variants.
SARS-CoV-2 and HIV-1 originate in animals and are transmitted from animal reservoirs to humans, including HIV.
Communicable Disease Programs: National Black Hiv/aids Awareness Day (nbhaad)
In their respective natural reservoirs, SARS-CoV-2 and HIV-1 infections cause few or no symptoms, but cause disease when they infect humans.
One of the reasons for the spread of the COVID-19 and AIDS epidemics is the transmission of SARS-CoV-2 and HIV-1 through asymptomatic infected people.
Lymphopenia due to severe loss of CD4 + T cells occurs in HIV-1 and SARS-CoV-2 infections and is considered a prognostic marker [ 45 , 46 , 47 ]. Compared to the chronic phase, the acute phase of HIV infection has a significant decrease in the number of CD4 + T cells, when the number of CD4 + T cells continues to decrease, and AIDS results. Lymphocytopenia is a marker of the severity of COVID-19, but elevated CD4+ T and CD8+ T cell levels are associated with mild disease.
SARS-CoV-2 and HIV-1 induce neutrophil extracellular traps (NETs) and NETosis, a mechanism of neutrophil death. Netosis can also cause increased secretion of chemokines and cytokines, leading to increased inflammation.
Hiv And Aids
In patients infected with SARS-CoV-2 and HIV-1, elevated serum levels of pro-inflammatory cytokines are considered biomarkers and prognostic variables related to morbidity and mortality.
Infection with two of these viruses, SARS-CoV-2 and HIV-1, results in immune dysregulation and is mediated by inflammasome activation. These viruses can activate the NLRP3 inflammasome in a variety of cells, including monocytes/macrophages and microglia. SARS-CoV-2-induced NLRP3 inflammasome macrophage and microglia activation in the central nervous system leads to neuroinflammation leading to several neurological manifestations.
In addition to systemic infection and immune suppression, HIV-1 also infects the central nervous system and causes neurodegenerative disease. HIV-1 infection of the central nervous system was identified early in the HIV-1 epidemic [ 30 , 48 , 49 ]. The presence of HIV-1 in cerebrospinal fluid and brain tissue during primary systemic infection may be associated with HIV infection during primary systemic infection. Despite controversy as to how HIV-1 enters the brain, the Trojan horse mechanism of HIV infection involves monocyte and lymphocyte trafficking and penetration of the blood-brain barrier (BBB). [54, 55, 56] Thus, HIV-1 neuroinvasion occurs primarily through immune cell trafficking across the BBB and then spreads through perivascular macrophage/monocyte and lymphocyte infection [25, 50, 53, 57, 58]. HIV-1 does not infect nerve cells. Neurological damage caused by HIV. Efficient viral replication creates a persistent inflammatory environment that leads to persistent neuroinflammation [59, 60], leading to the pathogenesis of HAND [59, 60]. The development and pathogenesis of HAND can also occur as a result of reactivation of the HIV-1 reservoir in the body.