A spotlight on HCV and SARS-CoV-2 co-infection and brain function.
A spotlight on HCV and SARS-CoV-2 co-infection and brain function.
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DOI：
10.1016/j.pbb.2022.173403
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发表时间：
2022-06
影响因子：
3.6
通讯作者：
Loftis, Jennifer M.
中科院分区：
文献类型：
--
作者：
Shirley, Kate;Loftis, Jennifer M.
与致病性RNA病毒（包括丙型肝炎病毒（HCV）和严重急性呼吸综合征冠状病毒-2（SARS-CoV-2））的共感染可影响疾病严重程度和临床结果（Dev i等人，2021年）。关于HCV感染对2019冠状病毒病（COVID-19）患者结局的影响的数据有限，并且没有关于具有COVID-19相关长期症状（长期COVID综合征; SARS CoV-2感染后急性后遗症[PASC]）的患者结局的数据。已经报道了与SARS-CoV-2感染相关的肝损伤（例如，Weber等人，2021年），但缺乏关于既存HCV感染对COVID-19结果影响的证据。认知障碍和神经精神功能障碍是两种HCV的记录后遗症（Adinolfi等人，2015; Hilsabec k等人，2002; Huckans等人，2009; Yarlott等人，2017）和长期COVID综合征（Frontera等人，2021; Graham等人，2021），但对合并感染对中枢神经系统（CNS）的后果和相关的神经精神结局知之甚少。由于合并感染可能会改变治疗和预后，因此关注HCV和SARS-CoV-2合并感染的神经和神经精神表现对于疾病监测和制定优化治疗的循证策略至关重要。各种免疫因子（细胞因子、趋化因子）和细胞（内皮细胞、T细胞）在共感染期间显示出失调，这增强了疾病的严重性，如肝纤维化和肝细胞炎症（Roe和Hall，2008; Zignego等人，2012年）; HIV发展为获得性免疫缺陷综合征（AIDS）（Chew和Bhattacharya，2016; Operskalski和Kovacs，2011）; CNS病理学（Jarvis等人，2013; Okurut等人，2020）;和神经精神障碍（Abdoli等人，2020年）。一般而言，合并感染可能对疾病结果有害、无关紧要或有帮助，考虑到COVID-19大流行，这一点尤为重要。共感染的影响取决于病原体之间的相互作用的类型，其可以是阳性或阴性的（McArdle等人，2018年; Li等人，2021年）。当病原体协同作用并导致疾病症状、严重程度和结果恶化时，发生积极的相互作用（Kehe et al.，2021年）。当一种病原体通过竞争、寄生或干扰阻碍另一种病原体的生长时，发生负相互作用（例如，霍夫曼等人，2006年）。负相互作用可导致短暂的保护作用，如在甲型流感病毒（IAV）和鼻病毒（RV）之间观察到的那样。Nickbakhsh等人（2019）证明，干扰素（IFN）可能诱导的负相互作用（Isaacs和Burke，1959）有助于我们观察到的IAV和RV的异步季节性模式。在病毒感染期间，一种病原体可能影响另一种病原体引起的复制和疾病严重程度。这被称为病毒干扰，并导致一种感染的早期清除和另一种感染的持续（Kumar等人，2018年）。除了共感染病原体之间的相互作用外，宿主反应在确定共感染的结果中也起着关键作用。宿主的反应取决于多种因素，包括人口统计学（例如，年龄），心理学（例如，压力），遗传，环境和其他因素。
Co-infection with pathogenic RNA viruses, including hepatitis C virus (HCV) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), can affect disease severity and clinical outcomes (Dev i et al., 2021). There are limited data on the effects of HCV infection on outcomes in individuals with coronavirus disease 2019 (COVID-19), and no data on outcomes in individuals with long-term symptoms associated with COVID-19 (long COVID syndrome; post-acute sequelae of SARS CoV-2 infection [PASC]). Liver injury has been reported in association with SARS-CoV-2 infection (eg, Weber et al., 2021), but evidence is lacking regarding the impact of pre-existing HCV infection on COVID-19 outcomes. Cognitive impairment and neuropsychiatric dysfunction are documented sequelae of both HCV (Adinolfi et al., 2015; Hilsabec k et al., 2002; Huckans et al., 2009; Yarlott et al., 2017) and long COVID syndrome (Frontera et al., 2021; Graham et al., 2021), but little is known about the consequences of co-infection on central nervous system (CNS) and related neuropsychiatric outcomes. Since co-infection may alter both treatment and prognosis, attention to the neurological and neuropsychiatric manifestations of HCV and SARS-CoV-2 co-infection is critical in disease surveillance and development of evidence-based strategies that optimize treatment. Various immune factors (cytokines, chemokines) and cells (endothelial cells, T cells) show dysregulation during co-infection, which enhances disease severity such as liver fibrosis and hepatocyte inflammation (Roe and Hall, 2008; Zignego et al., 2012); the progression of HIV to Acquired Immunodeficiency Syndrome (AIDS)(Chew and Bhattacharya, 2016; Operskalski and Kovacs, 2011); CNS pathology (Jarvis et al., 2013; Okurut et al., 2020); and neuropsychiatric disorders (Abdoli et al., 2020). In general, co-infections can be harmful, insignificant, or helpful for disease outcomes, and this is particularly important to consider given the COVID-19 pandemic. The effects of co-infection depend on the type of interactions between pathogens, which can be positive or negative (McArdle et al., 2018; Li et al., 2021). Positive interactions occur when pathogens act synergistically and lead to worsening of disease symptoms, severity, and outcomes (Kehe et al., 2021). Negative interactions occur when one pathogen hinders the growth of another pathogen through competition, parasitism, or interference (eg, Hoffman et al., 2006). Negative interactions can result in short-lived protective effects, as has been observed between influenza A virus (IAV) and rhinoviruses (RV). Nickbakhsh et al.(2019) demonstrated that negative interactions, potentially induced by interferon (IFN)(Isaacs and Burke, 1959), contribute to the asynchronous seasonal patterns we observe for IAV and RV. During viral infections, one pathogen may influence the replication and disease severity caused by the other. This is known as viral interference and leads to early clearance of one infection and persistence of the other one (Kumar et al., 2018). In addition to interactions between co-infecting pathogens, host response also plays a key role in determining the outcome of co-infections. The host response depends on multiple factors, including demographic (eg, age), psychological (eg, stress), genetic, environmental, and other factors.
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影响因子：
5
作者：
Gadotti AC;de Castro Deus M;Telles JP;Wind R;Goes M;Garcia Charello Ossoski R;de Padua AM;de Noronha L;Moreno-Amaral A;Baena CP;Tuon FF
通讯作者：
Tuon FF
影响因子：
2.5
作者：
Loftis, Jennifer M.;Huckans, Marilyn;Hauser, Peter
通讯作者：
Hauser, Peter
影响因子：
3.9
作者：
McArdle AJ;Turkova A;Cunnington AJ
通讯作者：
Cunnington AJ
影响因子：
4.4
作者：
Frontera JA;Yang D;Lewis A;Patel P;Medicherla C;Arena V;Fang T;Andino A;Snyder T;Madhavan M;Gratch D;Fuchs B;Dessy A;Canizares M;Jauregui R;Thomas B;Bauman K;Olivera A;Bhagat D;Sonson M;Park G;Stainman R;Sunwoo B;Talmasov D;Tamimi M;Zhu Y;Rosenthal J;Dygert L;Ristic M;Ishii H;Valdes E;Omari M;Gurin L;Huang J;Czeisler BM;Kahn DE;Zhou T;Lin J;Lord AS;Melmed K;Meropol S;Troxel AB;Petkova E;Wisniewski T;Balcer L;Morrison C;Yaghi S;Galetta S
通讯作者：
Galetta S
影响因子：
4.7
作者：
Lyra E Silva NM;Barros-Aragão FGQ;De Felice FG;Ferreira ST
通讯作者：
Ferreira ST