Considerable evidence indicate that HERVs can be reactivated by viral infections, such as:
1) retroviruses – human immunodeficiency virus type-1 (HIV-1), human T-lymphotropic virus 1 (HTLV-1);
2) RNA viruses – influenza A virus, hepatitis C virus (HCV), severe acute respiratory syndrome coronavirus-2 (SARSCoV-2);
3) DNA viruses – herpes simplex virus type-1 (HSV-1), Epstein-Barr virus (EBV), human cytomegalovirus (CMV), Kaposi’s sarcoma-associated herpesvirus (KSHV) 
Several studies have shown that EBV is able to transactivate the expression of the normally inactive HERV-K18 Env protein, e.g., interacting with resting B cells via CD21 receptor. Further studies revealed that the mechanism of transactivation depends on the expression of the major EBV late gene transactivator, EBNA-2. In-depth analysis completed the picture identifying the EBV latent membrane protein LMP-2A as a strong candidate for the HERV-K18 transactivation. HERV-K18 has also been reported to have superantigen activity (i.e. polyclonal T and B cell activation regardless of the specificity of their antigen receptor).
It has also been shown that in vitro binding of the EBV gp350 protein caused activation of MSRVenv and syncytin-1 in B-cells, monocytes, macrophages and in astrocytes - cells that are involved in pathogenesis of multiple sclerosis. Monocytes, especially after their differentiation into macrophages, appeared to be the most responsive to EBVgp350, expressing even higher levels of HERV-Wenv than B cells. This finding is concordant with another study, which demonstrated that during infectious mononucleosis EBV promoted the strongest activation of HERV-W/MSRV expression in monocytes compared to other blood cell types.