Virus-Encoded Complement Regulators: Current Status

Sinha, Anwesha; Singh, Anup K.; Kadni, Trupti Satish; Mullick, Jayati; Sahu, Arvind

doi:10.3390/v13020208

Cited by 11 publications

(3 citation statements)

References 159 publications

(219 reference statements)

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“…3 B). Several viruses, such as poxviruses, SARS-CoV-2, and KSHV, achieve immune escape using targeted proteins in the complement system [ 74 , 75 ]. In the present study, MASP1 , as a key molecule of the MBL pathway in the complement system, could induce immune responses after activation [ 76 ].…”

Section: Discussionmentioning

confidence: 99%

Proteins in pregnant swine serum promote the African swine fever virus replication: an iTRAQ-based quantitative proteomic analysis

Yang

Yuan

Hao

et al. 2023

Virol J

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African swine fever (ASF) is a severe infectious disease caused by the African swine fever virus (ASFV), seriously endangering the global pig industry. ASFV possesses a large genome, strong mutation ability, and complex immune escape mechanisms. Since the first case of ASF was reported in China in August 2018, it has had a significant impact on social economy and food safety. In the present study, pregnant swine serum (PSS) was found to promote viral replication; differentially expressed proteins (DEPs) in PSS were screened and identified using the isobaric tags for relative and absolute quantitation technology and compared with those in non-pregnant swine serum (NPSS). The DEPs were analyzed using Gene Ontology functional annotation, Kyoto Protocol Encyclopedia of Genes and Genome pathway enrichment, and protein–protein interaction networks. In addition, the DEPs were validated via western blot and RT-qPCR experiments. And the 342 of DEPs were identified in bone marrow-derived macrophages cultured with PSS compared with the NPSS. The 256 were upregulated and 86 of DEPs were downregulated. The primary biological functions of these DEPs involved signaling pathways that regulate cellular immune responses, growth cycles, and metabolism-related pathways. An overexpression experiment showed that the PCNA could promote ASFV replication whereas MASP1 and BST2 could inhibit it. These results further indicated that some protein molecules in PSS were involved in the regulation of ASFV replication. In the present study, the role of PSS in ASFV replication was analyzed using proteomics, and the study will be provided a basis for future detailed research on the pathogenic mechanism and host interactions of ASFV as well as new insights for the development of small-molecule compounds to inhibit ASFV.

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Section: Discussionmentioning

confidence: 99%

Proteins in pregnant swine serum promote the African swine fever virus replication: an iTRAQ-based quantitative proteomic analysis

Yang

Yuan

Hao

et al. 2023

Virol J

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“…The most striking evidence supporting the importance of C in viral infection outcome is provided by the evolution of specific evasion mechanisms employed by viruses for subverting C ( 55 ). First of all, viruses can recruit and exploit soluble and membrane-bound host C regulators, as well as encode their own C regulatory proteins ( 56 ). Moreover, they are also capable of using C regulators and receptors for cellular entry or even to modulate C protein expression through the upregulation of C regulators or the downregulation of C activators ( 57 ).…”

Section: Role Of Complement System In Viral Infections Including Sars-cov-2mentioning

confidence: 99%

COVID-19, Pre-Eclampsia, and Complement System

et al. 2021

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COVID-19 is characterized by virus-induced injury leading to multi-organ failure, together with inflammatory reaction, endothelial cell (EC) injury, and prothrombotic coagulopathy with thrombotic events. Complement system (C) via its cross-talk with the contact and coagulation systems contributes significantly to the severity and pathological consequences due to SARS-CoV-2 infection. These immunopathological mechanisms overlap in COVID-19 and pre-eclampsia (PE). Thus, mothers contracting SARS-CoV-2 infection during pregnancy are more vulnerable to developing PE. SARS-CoV-2 infection of ECs, via its receptor ACE2 and co-receptor TMPRSS2, can provoke endothelial dysfunction and disruption of vascular integrity, causing hyperinflammation and hypercoagulability. This is aggravated by bradykinin increase due to inhibition of ACE2 activity by the virus. C is important for the progression of normal pregnancy, and its dysregulation can impact in the form of PE-like syndrome as a consequence of SARS-CoV-2 infection. Thus, there is also an overlap between treatment regimens of COVID-19 and PE. C inhibitors, especially those targeting C3 or MASP-2, are exciting options for treating COVID-19 and consequent PE. In this review, we examine the role of C, contact and coagulation systems as well as endothelial hyperactivation with respect to SARS-CoV-2 infection during pregnancy and likely development of PE.

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“…The C9-mediated killing of bacteria in the absence of C5b-8 has also been reported (Dankert and Esser, 1987). Certain viruses also target complement component C9 as a complement evasion strategy (Bayly-Jones et al, 2017;Kim et al, 2013;Sinha et al, 2021). In humans, deficiency of the C9 component (C9D) is a rare genetic disorder (MIM: 120940) largely prevalent in Japan and Korea, possibly due to a founder event (Khajoee et al, 2003).…”

Section: Introductionmentioning

confidence: 98%