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2. Encephalitis And Its Unforeseen Effects On West Ham

2. Encephalitis And Its Unforeseen Effects On West Ham

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2. Encephalitis And Its Unforeseen Effects On West Ham

Feature papers represent the most advanced research with significant potential for major impact in the field. A feature paper should be a sufficiently original article that incorporates multiple techniques or approaches, provides an outlook on future research directions, and describes possible research applications.

Neurological Complications And Infection Mechanism Of Sars Cov 2

Special articles are submitted at the personal invitation or recommendation of scientific editors and must be positively assessed by the reviewers.

Editor’s Choice articles are based on recommendations from academic journal editors around the world. The editors select a small number of recently published articles in the journal that they believe are of particular interest to readers or relevant to a related area of ​​research. The aim is to provide an overview of some of the most exciting work published in the journal’s various research areas.

By Debashis Dutta Debashis Dutta Scilit Preprints.org Google Scholar View Publishing * , Jianuo Liu Jianuo Liu Scilit Preprints.org Google Scholar View Publishing and Huangui Xiong Huangui Xiong Scilit Preprints.org Google Scholar View Publishing *

Department of Pharmacology and Experimental Neuroscience, College of Medicine, Nebraska Medical Center, Omaha, NE 68198-5880, USA

A New Avenue For Lithium: Intervention In Traumatic Brain Injury

Received: April 12, 2023 / Revised: May 1, 2023 / Accepted: May 2, 2023 / Published: May 5, 2023

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of pandemic coronavirus disease 2019 (COVID-19), a fatal respiratory illness. Associated risk factors for Covid-19 include advanced age and medical comorbidities. In the current era of combination antiretroviral therapy (cART), a large proportion of people living with HIV-1 (PLWH) controlled viremia are elderly and have comorbidities, putting these people at risk of SARS-CoV-2 infection and Covid-19. 19 are exposed. associated serious consequences. In addition, SARS-CoV-2 is neurotropic and causes neurological complications, negatively affecting the health burden and people living with HIV, and aggravating HIV-1-associated neurocognitive disorder (HAND). The effects of SARS-CoV-2 infection and the severity of COVID-19 on neuroinflammation, the development of HAND and pre-existing HAND are not yet sufficiently understood. In this review, we have summarized the current knowledge about the differences and similarities between SARS-CoV-2 and HIV-1, the status of SARS-CoV-2/COVID-19 and HIV-1/AIDS syndemics, and their impact. Central nervous system (CNS). Risk factors for COVID-19 in people with HIV and neurological manifestations, inflammatory mechanisms leading to neurological syndromes, development of HAND and its impact on pre-existing HAND are also discussed. Finally, we examined the current syndemic challenges in the global population, with a particular focus on people living with HIV.

The world is in the midst of a debilitating coronavirus disease 2019 (COVID-19) pandemic that overlaps with the acquired immunodeficiency syndrome (AIDS) epidemic [1, 2, 3]. The causative agent of Covid-19 is the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and in AIDS the human immunodeficiency virus type 1 (HIV-1) [4, 5, 6, 7, 8]. There are more than 758 million SARS-CoV-2 infections worldwide, with over 6.8 million deaths attributed to Covid-19 [9]. However, a total of 84.2 million people are infected with HIV-1 and 4.1 million have died from AIDS-related diseases. In 2021, the total number of people living with HIV-1 (PLWH) was 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 a co-epidemic or syndemic of SARS-CoV-2/COVID-19/and HIV-1/AIDS [12, 13]. It has been hypothesized that people living with HIV are at high risk of SARS-CoV-2 infection and its consequences due to their dysregulated immune and inflammatory states, but a clear consensus is lacking [ 13 , 14 , 15 , 16 , 17 , 18 ]. The absence of high risk may be due to combination antiretroviral therapy (CART), which suppresses viral load and immune reconstitution status. However, global reports have revealed severe clinical symptoms and increased morbidity and mortality of SARS-CoV-2 infection in people with HIV compared to people without HIV-1 [19, 20, 21, 22, 23]. In addition to respiratory syndrome, COVID-19 triggers neurological manifestations such as headache, confusion, impaired consciousness, anosmia, aesthetics, meningoencephalitis, neuropsychiatric disorders and others [24, 25, 26, 27]. Therefore, the onset of Covid-19-related neurological manifestations may lead to cumulative neurological manifestations in PLHIV and individuals who have progressed to HIV-1-associated neurocognitive disorders (HAND) [28, 29].

HIV-1 central nervous system (CNS) invasion was discovered early in the HIV-1 epidemic, and brain infections have been well studied and characterized, as have viral proteins and their neurotoxicity [30, 31, 32]. Current evidence suggests that SARS-CoV-2 invades the CNS and modulates the host immune response, leading to neurological manifestations [33, 34, 35]. Post-acute sequelae of SARS-CoV-2 (PASC) or long-COVID have been found to have a negative impact on people living with HIV, particularly in people with HAND [36, 37]. This review presents recent advances in the neurological manifestations of SARS-CoV-2/COVID-19 in people living with HIV with or without hands. It covers similarities and differences between SARS-CoV-2 and HIV-1; SARS-CoV-2-induced neurological manifestations, including learning from HIV-1-induced neurological consequences; Presents the risk factors of Covid-19 in people living with HIV and the neurological impact of SARS-CoV-2/COVID-19 and HIV-1/AIDS syndemics. and exploring plausible mechanisms underlying neurological outcomes in PLHIV with SARS-CoV-2 infection and individuals with HAND, with a focus on neurotoxicity associated with overactivation of the NLRP3 inflammasome [38, 39]. It also discusses the challenges of Covid-19 among people living with HIV, including PASC and ongoing Covid events, as well as possible ways to overcome the overwhelming impact of the SARS-CoV-2/HIV-1 syndemic.

Climate, Ecology, And Infectious Disease

SARS-CoV-2 and HIV-1 are natural RNA viruses that are transmitted to humans through zoonotic transmission [40, 41]. Despite the differences, these viruses utilize common molecular mechanisms during transmission and disease progression [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.

The most common feature of SARS-CoV-2 and HIV-1 viral infections is panic in the population. This public fear makes people mentally ill and causes stress and anxiety [42].

Both the genomes of SARS-CoV-2 and HIV-1 are susceptible to mutations, and the accumulation of mutations within hosts under selection pressure leads to the emergence of new variants. Furthermore, immunosuppressed people with HIV harbor SARS-CoV-2 for extended periods of time, allowing sufficient time for the accumulation of mutants and the resulting derivation of the SARS-CoV-2 variant [44].

SARS-CoV-2 and HIV-1 are of zoonotic origin and have been transmitted to humans from animal hosts, HIV-1 from non-human primates (NHPs), and SARS-CoV-2 from bats.

Priming With Japanese Encephalitis Virus Or Yellow Fever Virus Vaccination Led To The Recognition Of Multiple Flaviviruses Without Boosting Antibody Responses Induced By An Inactivated Zika Virus Vaccine

In their respective natural reservoirs, SARS-CoV-2 and HIV-1 infections cause mild or no symptoms, but cause disease when infected in humans.

One cause of the widespread COVID-19 and AIDS epidemics is the asymptomatic transmission of SARS-CoV-2 and HIV-1 by infected individuals.

Lymphopenia occurs as a result of severe loss of CD4 + T cells due to HIV-1 and SARS-CoV-2 infection and is considered a prognostic marker [ 45 , 46 , 47 ]. The number of CD4+ T cells is significantly reduced during the acute phase of HIV-1 infection, in contrast to the chronic phase in which CD4+ T cells continually decrease, leading to AIDS. Lymphocytopenia is a hallmark of COVID-19 severity, but higher levels of CD4+T and CD8+T cells were associated with milder disease states [ 45 ].

SARS-CoV-2 and HIV-1 induce neutrophil extracellular traps (NETs) and cause NETosis, a death mechanism for neutrophils. Netosis can also increase the secretion of chemokines and cytokines, leading to increased inflammation.

Neuroimaging Manifestations In Children With Sars Cov 2 Infection: A Multinational, Multicentre Collaborative Study

Elevated serum levels of proinflammatory cytokines in SARS-CoV-2 and HIV-1 infected patients are considered biomarkers and are predictive variables associated with morbidity and mortality.

Infection with these two viruses, SARS-CoV-2 and HIV-1, leads to immune changes and is mediated by the activation of inflammasomes. These viruses can activate the NLRP3 inflammasome in various cells, including monocytes/macrophages and microglia. SARS-CoV-2-induced activation of the microglial and macrophage NLRP3 inflammasome in the CNS leads to neuroinflammation, leading to numerous neurological manifestations.

In addition to systemic infection and immunosuppression, HIV-1 infects the CNS and causes neurological manifestations. CNS infection with HIV-1 was identified early in the HIV-1 epidemic [30, 48, 49]. The presence of HIV-1 in CSF and brain tissue within days of primary systemic infection suggests HIV-1 neuroinvasion early in the infection [49, 50, 51, 52, 53]. Despite the controversy over how HIV-1 enters the brain, the Trojan horse mechanism of HIV-1 infection of monocytes and lymphocyte trafficking and penetration of the blood-brain barrier (BBB) ​​is linked to CNS disease. infection most convincing [54, 55, 56]. Thus, HIV-1 neuroinvasion occurs primarily through transport of immune cells across the blood-brain barrier, followed by transmission through infection of perivascular macrophages/monocytes and lymphocytes [25, 50, 53, 57, 58]. HIV-1 does not infect neurons. Neuronal damage is thought to be mediated by HIV-associated neuroinflammation and neurotoxic viral proteins (gp120, Tat, Nef and Vpr). Abundant viral replication generates a prolonged inflammatory environment, leading to persistent neuroinflammation [59, 60] and leading to the pathogenesis of HAND [59, 60]. The pathogenesis and progression of HAND may also be due to the reactivation of HIV-1 reservoirs.

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    1. 2. Encephalitis And Its Unforeseen Effects On West HamFeature papers represent the most advanced research with significant potential for major impact in the field. A feature paper should be a sufficiently original article that incorporates multiple techniques or approaches, provides an outlook on future research directions, and describes possible research applications.Neurological Complications And Infection Mechanism Of Sars Cov 2Special articles are submitted at the personal invitation or recommendation of scientific editors and must be positively assessed by the reviewers.Editor's Choice articles are based on recommendations from academic journal editors around the world. The editors select a small number of recently published articles in the journal that they believe are of particular interest to readers or relevant to a related area of ​​research. The aim is to provide an overview of some of the most exciting work published in the journal's various research areas.By Debashis Dutta Debashis Dutta Scilit Preprints.org Google Scholar View Publishing * , Jianuo Liu Jianuo Liu Scilit Preprints.org Google Scholar View Publishing and Huangui Xiong Huangui Xiong Scilit Preprints.org Google Scholar View Publishing *Department of Pharmacology and Experimental Neuroscience, College of Medicine, Nebraska Medical Center, Omaha, NE 68198-5880, USAA New Avenue For Lithium: Intervention In Traumatic Brain InjuryReceived: April 12, 2023 / Revised: May 1, 2023 / Accepted: May 2, 2023 / Published: May 5, 2023Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of pandemic coronavirus disease 2019 (COVID-19), a fatal respiratory illness. Associated risk factors for Covid-19 include advanced age and medical comorbidities. In the current era of combination antiretroviral therapy (cART), a large proportion of people living with HIV-1 (PLWH) controlled viremia are elderly and have comorbidities, putting these people at risk of SARS-CoV-2 infection and Covid-19. 19 are exposed. associated serious consequences. In addition, SARS-CoV-2 is neurotropic and causes neurological complications, negatively affecting the health burden and people living with HIV, and aggravating HIV-1-associated neurocognitive disorder (HAND). The effects of SARS-CoV-2 infection and the severity of COVID-19 on neuroinflammation, the development of HAND and pre-existing HAND are not yet sufficiently understood. In this review, we have summarized the current knowledge about the differences and similarities between SARS-CoV-2 and HIV-1, the status of SARS-CoV-2/COVID-19 and HIV-1/AIDS syndemics, and their impact. Central nervous system (CNS). Risk factors for COVID-19 in people with HIV and neurological manifestations, inflammatory mechanisms leading to neurological syndromes, development of HAND and its impact on pre-existing HAND are also discussed. Finally, we examined the current syndemic challenges in the global population, with a particular focus on people living with HIV.The world is in the midst of a debilitating coronavirus disease 2019 (COVID-19) pandemic that overlaps with the acquired immunodeficiency syndrome (AIDS) epidemic [1, 2, 3]. The causative agent of Covid-19 is the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and in AIDS the human immunodeficiency virus type 1 (HIV-1) [4, 5, 6, 7, 8]. There are more than 758 million SARS-CoV-2 infections worldwide, with over 6.8 million deaths attributed to Covid-19 [9]. However, a total of 84.2 million people are infected with HIV-1 and 4.1 million have died from AIDS-related diseases. In 2021, the total number of people living with HIV-1 (PLWH) was 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 a co-epidemic or syndemic of SARS-CoV-2/COVID-19/and HIV-1/AIDS [12, 13]. It has been hypothesized that people living with HIV are at high risk of SARS-CoV-2 infection and its consequences due to their dysregulated immune and inflammatory states, but a clear consensus is lacking [ 13 , 14 , 15 , 16 , 17 , 18 ]. The absence of high risk may be due to combination antiretroviral therapy (CART), which suppresses viral load and immune reconstitution status. However, global reports have revealed severe clinical symptoms and increased morbidity and mortality of SARS-CoV-2 infection in people with HIV compared to people without HIV-1 [19, 20, 21, 22, 23]. In addition to respiratory syndrome, COVID-19 triggers neurological manifestations such as headache, confusion, impaired consciousness, anosmia, aesthetics, meningoencephalitis, neuropsychiatric disorders and others [24, 25, 26, 27]. Therefore, the onset of Covid-19-related neurological manifestations may lead to cumulative neurological manifestations in PLHIV and individuals who have progressed to HIV-1-associated neurocognitive disorders (HAND) [28, 29].HIV-1 central nervous system (CNS) invasion was discovered early in the HIV-1 epidemic, and brain infections have been well studied and characterized, as have viral proteins and their neurotoxicity [30, 31, 32]. Current evidence suggests that SARS-CoV-2 invades the CNS and modulates the host immune response, leading to neurological manifestations [33, 34, 35]. Post-acute sequelae of SARS-CoV-2 (PASC) or long-COVID have been found to have a negative impact on people living with HIV, particularly in people with HAND [36, 37]. This review presents recent advances in the neurological manifestations of SARS-CoV-2/COVID-19 in people living with HIV with or without hands. It covers similarities and differences between SARS-CoV-2 and HIV-1; SARS-CoV-2-induced neurological manifestations, including learning from HIV-1-induced neurological consequences; Presents the risk factors of Covid-19 in people living with HIV and the neurological impact of SARS-CoV-2/COVID-19 and HIV-1/AIDS syndemics. and exploring plausible mechanisms underlying neurological outcomes in PLHIV with SARS-CoV-2 infection and individuals with HAND, with a focus on neurotoxicity associated with overactivation of the NLRP3 inflammasome [38, 39]. It also discusses the challenges of Covid-19 among people living with HIV, including PASC and ongoing Covid events, as well as possible ways to overcome the overwhelming impact of the SARS-CoV-2/HIV-1 syndemic.Climate, Ecology, And Infectious DiseaseSARS-CoV-2 and HIV-1 are natural RNA viruses that are transmitted to humans through zoonotic transmission [40, 41]. Despite the differences, these viruses utilize common molecular mechanisms during transmission and disease progression [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.The most common feature of SARS-CoV-2 and HIV-1 viral infections is panic in the population. This public fear makes people mentally ill and causes stress and anxiety [42].Both the genomes of SARS-CoV-2 and HIV-1 are susceptible to mutations, and the accumulation of mutations within hosts under selection pressure leads to the emergence of new variants. Furthermore, immunosuppressed people with HIV harbor SARS-CoV-2 for extended periods of time, allowing sufficient time for the accumulation of mutants and the resulting derivation of the SARS-CoV-2 variant [44].SARS-CoV-2 and HIV-1 are of zoonotic origin and have been transmitted to humans from animal hosts, HIV-1 from non-human primates (NHPs), and SARS-CoV-2 from bats.Priming With Japanese Encephalitis Virus Or Yellow Fever Virus Vaccination Led To The Recognition Of Multiple Flaviviruses Without Boosting Antibody Responses Induced By An Inactivated Zika Virus VaccineIn their respective natural reservoirs, SARS-CoV-2 and HIV-1 infections cause mild or no symptoms, but cause disease when infected in humans.One cause of the widespread COVID-19 and AIDS epidemics is the asymptomatic transmission of SARS-CoV-2 and HIV-1 by infected individuals.Lymphopenia occurs as a result of severe loss of CD4 + T cells due to HIV-1 and SARS-CoV-2 infection and is considered a prognostic marker [ 45 , 46 , 47 ]. The number of CD4+ T cells is significantly reduced during the acute phase of HIV-1 infection, in contrast to the chronic phase in which CD4+ T cells continually decrease, leading to AIDS. Lymphocytopenia is a hallmark of COVID-19 severity, but higher levels of CD4+T and CD8+T cells were associated with milder disease states [ 45 ].SARS-CoV-2 and HIV-1 induce neutrophil extracellular traps (NETs) and cause NETosis, a death mechanism for neutrophils. Netosis can also increase the secretion of chemokines and cytokines, leading to increased inflammation.Neuroimaging Manifestations In Children With Sars Cov 2 Infection: A Multinational, Multicentre Collaborative Study
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