The imitation game: a viral strategy to subvert the complement system

Agrawal, Palak; Sharma, Samriddhi; Pal, Pradipta; Ojha, Hina; Mullick, Jayati; Sahu, Arvind

doi:10.1002/1873-3468.13856

Cited by 16 publications

(9 citation statements)

References 170 publications

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“…These mutations may substantially impair the binding affinity of antibodies as we have outlined above 65 . On the other hand, viral immune evasion is also associated with the impairment of the non‐specific effector of humoral immunity, the complement system 66 . Some gene sequences in the viral genome are homologs encoding the complement regulatory proteins that could inhibit the activation of the complement system.…”

Section: Immune Evasion Of Sars‐cov‐2 Omicronmentioning

confidence: 99%

SARS‐CoV‐2 Omicron variant: Immune escape and vaccine development

Lan

et al. 2022

MedComm

109

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New genetic variants of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) constantly emerge through unmitigated spread of the virus in the ongoing Coronavirus disease 2019 pandemic. Omicron (B.1.1.529), the latest variant of concern (VOC), has so far shown exceptional spread and infectivity and has established itself as the dominant variant in recent months. The SARS‐CoV‐2 spike glycoprotein is a key component for the recognition and binding to host cell angiotensin‐converting enzyme 2 receptors. The Omicron variant harbors a cluster of substitutions/deletions/insertions, and more than 30 mutations are located in spike. Some noticeable mutations, including K417N, T478K, N501Y, and P681H, are shared with the previous VOCs Alpha, Beta, Gamma, or Delta variants and have been proven to be associated with higher transmissibility, viral infectivity, and immune evasion potential. Studies have revealed that the Omicron variant is partially resistant to the neutralizing activity of therapeutic antibodies and convalescent sera, which poses significant challenges for the clinical effectiveness of the current vaccines and therapeutic antibodies. We provide a comprehensive analysis and summary of the epidemiology and immune escape mechanisms of the Omicron variant. We also suggest some therapeutic strategies against the Omicron variant. This review, therefore, aims to provide information for further research efforts to prevent and contain the impact of new VOCs during the ongoing pandemic.

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Section: Immune Evasion Of Sars‐cov‐2 Omicronmentioning

confidence: 99%

SARS‐CoV‐2 Omicron variant: Immune escape and vaccine development

Lan

et al. 2022

MedComm

109

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“…An effective innate immune defense, therefore, must target both phases of the virus life cycle. Notably, all the major complement pathways-classical, alternative, and lectin-are potent in targeting cell-free viral particles as well as the virus-infected cells [34][35][36][37]. Moreover, as stated above, the system also boosts other antiviral innate [9] and acquired immune responses [7,8] to limit the viral infection.…”

Section: Viral Complement Regulatorsmentioning

confidence: 96%

Virus-Encoded Complement Regulators: Current Status

Sinha

Singh

Kadni

et al. 2021

Viruses

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Viruses require a host for replication and survival and hence are subjected to host immunological pressures. The complement system, a crucial first response of the host immune system, is effective in targeting viruses and virus-infected cells, and boosting the antiviral innate and acquired immune responses. Thus, the system imposes a strong selection pressure on viruses. Consequently, viruses have evolved multiple countermeasures against host complement. A major mechanism employed by viruses to subvert the complement system is encoding proteins that target complement. Since viruses have limited genome size, most of these proteins are multifunctional in nature. In this review, we provide up to date information on the structure and complement regulatory functions of various viral proteins.

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“…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 imitation game: a viral strategy to subvert the complement system

Cited by 16 publications

References 170 publications

SARS‐CoV‐2 Omicron variant: Immune escape and vaccine development

SARS‐CoV‐2 Omicron variant: Immune escape and vaccine development

Virus-Encoded Complement Regulators: Current Status

COVID-19, Pre-Eclampsia, and Complement System

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