“…Based on epidemiological and phylogenetic data, it has been hypothesized that HPyV co-evolved with their hosts, leading to high prevalence, low pathogenicity and symptom-less latency in immune competent settings [ 21 ]. HPyV tend to become latent post-primary infection and undergo reactivation among immune-compromised individuals, including HIV positive individuals, organ transplant patients, and individuals affected by autoimmune diseases [ 6 , 22 , 23 , 24 , 25 ]. Immunosuppressant conditions including pregnancy and chronic alcohol abuse are sufficient to lead to PyV reactivation [ 6 ].…”