Table 2.
Lipid mediators in viral infection.
| Mediator | Virus | Prohost/provirus | Mechanism | Reference |
|---|---|---|---|---|
| Class 1 | ||||
| PGE2a | HSV-1 | Provirus | Increase viral replication | (Harbour, Blyth and Hill 1978) |
| CMV | Provirus | -PGE2 contributes to immunosuppressive effect | (Nokta et al. 1996; Hooks et al. 2006; Schröer and Shenk 2008) | |
| -PGE2 increases plaque formation and viral DNA copy number | ||||
| -PGE2 plays a role in direct cell-to-cell spreading | ||||
| EBV | Provirus | Lytic reaction via EP signaling pathways | (Gandhi et al. 2015) | |
| Rotavirus | Provirus | Might be required for early infection, i.e. attachment | ||
| Enterovirus 71 | Provirus | PGE2 might be required for replication | (Tung, Hsieh and Yang 2010; Tung et al. 2011; Wang et al. 2015) | |
| Sapovirus | Provirus | PGE2 decreases the production of nitric oxide, leading to an increase in PSAV | (Alfajaro et al. 2017) | |
| VSV | Provirus | -COX inhibitors/antagonist reduced viral production, but the effect is overcome by exogenous PGE2 | (Chen, Warner and Reiss 2000; Chen, Restivo and Reiss 2002) | |
| -COX-2 antagonist decreased viral titers | ||||
| LCMV | Provirus | PGE2i inhibits the survival and effector functions of Tc | (Chen et al. 2015) | |
| HTLV-1 | Provirus | PGE2 causes an increased production of virus | (Kuno et al. 1986) | |
| MDV | Provirus | Promotes virus replication | (Boodhoo et al. 2019) | |
| IAV | Provirus | PGE2 inhibits type-I IFNs and apoptosis pathways | (Coulombe et al. 2014; Park et al. 2016) | |
| RSV | Provirus | PGE2 causes a delayed protective RSV specific immune response | (Bartz et al. 2002) | |
| Coxsackie virus | Prohost | Decrease viral titers | (Xie et al. 2012) | |
| HPIV-3 | Prohost | PGE2 inhibits viral replication | (Luczak et al. 1975) | |
| HBV | Prohost | -PGE2 results in loss of viral replication | (Flowers et al. 1994; Hyman et al. 1999) | |
| -PGE2 decreases viral antigen | ||||
| HIV | Prohost | -PGE2 decreases virion penetration by suppressing expression of CCR5 | (Thivierge et al. 1998; Hayes et al. 2002; Clemente et al. 2014) | |
| -PGE2 inhibits virus replication by protein kinase A-dependent mechanism | ||||
| -PGE2 reduces cell-to-cell spreading | ||||
| HIV | Provirus | -PGE2 enhances HIV-1 long terminal repeat mediated reporter gene activation | (Dumais, Barbeau and Olivier 1998; Fitzgerald et al. 2012; Zambrano-Zaragoza et al. 2014) | |
| -PGE2 has an immunosuppressive effect when co-infected with HPV | ||||
| -PGE2 could play a role in pathogenicity via Th17 cell regulation | ||||
| dmPGA1 | HSV-1 | Prohost | Significantly inhibited viral replication | (Hughes-Fulford et al. 1992) |
| HIV | Significantly inhibited viral replication | (Hughes-Fulford et al. 1992) | ||
| dmPGE2 | HSV | Provirus | Up to a 60% increase in HSV replication compared with that in untreated virus-infected cells | (Hughes-Fulford et al. 1992) |
| dmPGA2 | HSV | Provirus | Up to a 60% increase in HSV replication compared with that in untreated virus-infected cells | (Hughes-Fulford et al. 1992) |
| LTE4 | RSV | Provirus | Urinary LTE4 was 8-fold higher in infants with bronchiolitis than in controls | (Piedimonte et al. 2005) |
| LTB4a | HTLV-1 | Provirus | HTLV-1 infection dysregulates the LT pathway to promote viral replication | (Trindade et al. 2012; Percher et al. 2017) |
| CMV | Prohost | Significant reduction in viral titers | (Gaudreault and Gosselin 2007) | |
| IAV | Prohost | Significant decrease in lung viral loads | (Gaudreault and Gosselin 2008) | |
| HIV | Prohost | LTB4 induced the secretion alpha defensins and MIP-1 beta to activate neutrophils | (Flamand et al. 2004) | |
| EBV | Prohost | LTB4 can induce T-cell activation that inhibits the EBV-induced proliferation of B lymphocytes | (Liu et al. 2008) | |
| Influenza B | Prohost | Significant reduction in viral titers | (Widegren et al. 2011) | |
| Coronavirus | Prohost | Significant reduction in viral titers | (Widegren et al. 2011) | |
| RSV | Prohost | Significant reduction in viral titers | (Widegren et al. 2011) | |
| HSV-1 | Prohost | Increase in antimicrobial proteins to restrict infection | (Flamand, Tremblay and Borgeat 2007) | |
| Class 2 | ||||
| PAFa | HIV | Provirus | Enhances replication | (Lima et al. 2006) |
| RSV | Provirus | Enhances the inflammatory environment | (Villani et al. 1991) | |
| DENV | Provirus | Induces an increase in vascular permeability, hypotension, and production of cytokines | (Souza et al. 2009) | |
| HCV | Provirus | A higher amount of plasma PAF level was observed in infected patients | (Caini et al. 2007) | |
| LPA | HCV | Provirus | Inhibiting LPA signaling reduced HCV replication | (Farquhar et al. 2017) |
| RSV | Provirus | Role in RSV filament formation and virus-induced cell-to-cell fusion | (Gower et al. 2005) | |
| S1Pa | IAV | Provirus | Overexpression of S1P heightened the cells' susceptibility to influenza virus infection | (Seo et al. 2010; Zhao et al. 2019) |
| HSV-1 | Provirus | Facilitates successful HSV-1 replication | (Graber et al. 2020) | |
| DENV | Prohost | Low S1P levels correlated with exaggerated DENV replication | (Gomes et al. 2014; Michels et al. 2015) | |
| Class 3 | ||||
| PD1 | IAV (H5N1) | Prohost | PD1 treatment improved the survival and pathology of severe influenza in mice, decreases in TNF-α and IFN-γ | (Morita et al. 2013) |
| HSV-1 | Prohost | NPD1 significant reduction in the severity and incidence of HSV-induced stromal keratitis | (Rajasagi et al. 2013) | |
| Lipoxina | IAV (H5N1) | Prohost | TNFα and interferon-γ were found to be upregulated | (Cilloniz et al. 2010) |
| RSV | Prohost | Promotes differentiation of alternatively activated macrophages and helps resolve airway hyperreactivity | (Richardson et al. 2005; Shirey et al. 2014) | |
| KSHV | Prohost | Creates an anti-inflammatory environment by decreasing the levels of NF-κB, AKT, ERK1/2, COX-2 and 5-lipoxygenase | (Chandrasekharan et al. 2016) | |
| RvE1 | HSV-1 | Prohost | Reduces proinflammatory mediators and stimulates IL-10 | (Rajasagi et al. 2011) |
| RSV | Prohost | Restored the alternatively activated macrophage phenotype | (Shirey et al. 2014) | |
a
Found to be produced from LDs or influence LD biogenesis.
Abbreviations: HIV-1: Human immunodeficiency virus 1; CMV: Cytomegalovirus; EBV: Epstein–Barr virus; VSV: Vesicular stomatitis virus; LCMV: Lymphocytic choriomeningitis virus; HTLV-1: Human T-lymphotropic virus 1; MDV: Marek's Disease Virus; IAV: Influenza A virus; RSV: Respiratory syncytial virus; HPIV-3: Human parainfluenza virus-3; HBV: Hepatitis B; DENV: Dengue virus; and KSHV: Kaposi's sarcoma-associated herpesvirus.