| Virus* (genome, family) |
Macrophage-related primary infection cells/sites |
Effect of manipulation/infection in monocytes, MΦs and DCs |
Reference |
| DENV ((+)ssRNA, Flaviviridae) |
Monocytes, MΦs and DCs in multiple tissues of IFN-αβγR KO mice |
MΦ-depletion: Tenfold increase in systemic viral titer, and massive infiltration of monocytes |
[32,33] |
| RSV ((-)ssRNA, Paramyxoviridae) |
Blood monocytes, DCs, lung epithelial cells and MΦs in mice/humans |
MΦ-depletion: Abolished local inflammatory cytokine peak at 1 dpi, and enhanced viral load in the lung at 4 dpi |
[34,35] |
| HIV1 ((+)ssRNA, Retroviridae) |
Macrophages and T cells in humans |
Deficiency of CCR5, a co-receptor that mediates HIV macrophage-tropism, showed resistance to HIV-1infection |
[39,40] |
| WNV ((+)ssRNA, Flaviviridae) |
Murine keratinocytes and skin-resident DCs, and probable peripheral MΦs and DCs mediating neuroinvasion |
MΦ-depletion: Higher and extended viremia, and accelerated encephalitis and death. Inhibition of NOS activity of infiltrating MΦs relieved encephalitis and prolonged survival |
[41-43] |
| SARS-Cov((+)ssRNA, Coronaviridae) |
Human respiratory epithelial cells, and antibody-enhanced infection of macrophages and immune cells |
Depletion of alveolar MΦs 1-2 day before infection, (but not at 2 dpi), prevented lethal disease, and enhanced viral clearance |
[44,45] |
| IAV (Segmented (-)RNA, Orthomyxoviridae) |
Airway and lung epithelial cells, DCs, and MΦs of mice/humans/pigs |
MΦ-depletion: Strain-dependent exacerbation of viral replication, increased airway inflammation and viral pneumonia |
[36-38] |
| CSFV ((+)ssRNA, Flaviviridae) |
Porcine blood monocytes/macrophages |
Viral infection stimulated arginase-1 (ARG-1) but suppressed nitric oxide synthase (iNOS) expression, i.e., induced M1-M2 repolarization |
[50,51] |
| PrV (dsRNA, Hepesviridae) |
Porcine lung epithelial cells and MΦs and spread via infected blood monocytes |
Acute IFN-α response is important in diminishing the spread of PrV in the connective tissue but not in epithelial cells (IFN cell preferences) |
[52-54] |
| ASFV (dsRNA, Asfarviridae) |
Primarily and persistently infected tissuemonocytes/ MΦs and fibroblasts in multiple tissues |
Massive M1 polarization served as a modulator of the viral pathogenesis including pulmonary edema, hemorrhage, and lymphoid depletion that characterize the disease |
[55,56] |
| PCV2 (ssDNA, Cirvoviridae) |
Monocyte/MΦ lineage cells, including alveolar MΦs, are the major target cells |
Acute infection reduced alveolar MΦs phagocytosis and microbicidal capability; and persistence increased inflammatory and pro-apoptotic responses, which led to lymphopenia and immunosuppression |
[57,58] |
| FMDV((+)ssRNA, picornaviridae) |
Early infection of porcine T and B cells caused viremia; immunocomplex promoted productive infection and killing of mDCs |
Increase IL-10 production in infected DCs, loss of pDC cell function coincides with lymphopenia in FMDV-infected pigs; macrophage depletion in vaccinated mice severely decreased vaccine protection |
[59-63] |
| PRRSV ((+)ssRNA, Arteriviridae) |
Tissue macrophages, monocytes and mDCs especially those in reproductive and respiratory tracts. |
Massive cell death of infected monocytic cells; increase of IL-10 and reduction of phagocytic, microbicidal, pro-inflammatory, and antigen-presentation activity in MΦs and DCs. Pathogenicity-related suppression of IFN-α production in pDCs |
[64-66] |
| *ASFV: African Swine Fever Virus; CSFV: Classical Swine Fever Virus; DENV: Dengue Virus; FMDV:Foot and Mouth Disease Virus; HIV1:Human Immunodeficiency Virus 1; IAV:Influenza A Virus; PCV2:Porcine Circovirus-2; PRRSV: Porcine Reproductive and Respiratory Syndrome Virus; PrV:Porcine PseudorabiesVirus; RSV:Respiratory Syncytial Virus; SARS-Cov:Severe Acute Respiratory Syndrome Coronavirus; WNV:West Nile Virus |
