Table 1.
Interaction of complement proteins to viruses, and biological consequences.
| Virus | C1q Binding | Consequences of C1q Binding | MBL Binding | Consequences of MBL Binding | C4BP Binding | Consequences of C4BP Binding | Properdin Binding | Consequences of Properdin Binding | Factor H Binding | Consequences of Factor H Binding |
|---|---|---|---|---|---|---|---|---|---|---|
| Murine Leukaemia Virus (MuLV) | + | Complement activation Viral lysis by human serum | ? | |||||||
| Human Immunodeficiency Virus (HIV-1, 2) |
+ | Complement activation No virolysis by human serum Enhancement of infection of C receptor-bearing cells |
+ | In vitro inhibition of the virus Complement activation Enhancement of infection Virus uptake by macrophages |
? | + | + | Escape complement destruction | ||
| Human T Lymphotropic Virus (HTLV) | + | In vitro inhibition of the virus complement activation No virolysis by human serum |
+ | |||||||
| Herpes Simplex Virus 1 (HSV-1) | + | Neutralisation of a gC null virus by a C1–C5 dependent mechanism | ? | |||||||
| Herpes Simplex Virus 2 (HSV-2) | ? | + | Enhancement of infection in a murine model | |||||||
| Human gamma-herpesvirus 8 | + | Induces complement activation during de novo KSHV infection | ||||||||
| Epstein-Barr Virus (EBV) | + | Classical pathway activation No neutralisation of the virus Opsonisation of the virus |
? | |||||||
| Cytomegalovirus (CMV) | + | Classical pathway activation No lysis of infected cells |
- | |||||||
| Influenza A Virus (IAV) | + | + | C-independent virus inactivation Complement activation (guinea pig) | + | Differentially modulates the efficacy of viral entry and replication in a strain-dependent manner | + | Differentially modulates the efficacy of viral entry and replication in a strain-dependent manner | + | Differentially modulates the efficacy of viral entry and replication in a strain-dependent manner | |
| Flavivirus | + | Viral NS1 limits complement activation by binding C4BP | + | Enhance complement activation | Enables immune evasion | |||||
| Hepatitis B virus | + | Upregulates C4BPα through transcription factor Sp1 inhibiting complement activation | ||||||||
| Adenovirus | + | Increased uptake by hepatocytes Reduced hepatic and innate toxicity after systemic application of adenoviruses vector |
||||||||
| Sindbis virus | + | Reduced alternative pathway activation | ||||||||
| SARS CoV 2 | ? | Lower C1q levels in the blood of severely ill patients Localised deposits of C1q in lungs suggesting classical pathway activation |
? | N-protein of SARS-CoV-2 has been shown to interact with (MASP2) | ? | ? | ? | The addition of factor H help mitigate damages caused by uncontrolled alternative pathway activation by viral S1/S2 protein |