Last week, we learned that after primary infection and subsequent symptoms, Human Herpesvirus Six (HHV-6) as well as other members of the herpesviridae family remains latent until the host undergoes stress or becomes immunocompromised. In the latter case, herpesviruses become highly virulent, causing morbidity and mortality in patients. With organ transplant recipients receiving drugs, complications such as “marrow suppression, pneumonitis, encephalitis, hepatitis, fever, and an eruption [?]” may lead to “organ rejection and death” . With the case of HIV+ patients, however, a peculiar situation arises in which HHV-6 targets the same cell in the body as the immunodeficiency virus that could potentially reactivate it. Below are two articles showing that HIV-1/HHV-6 coinfection presents in different ways for different cells: whereas the two articles agree that in a CD4+ cell infected with both viruses, HHV-6 can promote the expression of HIV-1, thus making it more pathogenic, the second article  suggest that HHV-6 could also suppress HIV-1 activity in dendritic cells, which supposedly plays “an important role in the immunopathogenesis [HIV]” . The anti-HIV effect of HHV-6 may be related to the down-regulating of HIV-specific surface proteins, but [I haven’t done enough research to be specific]. What all of this suggests is that HHV-6, a very common virus that infects ~100% of the population can possibly be used as a weapon against HIV. Further research into inhibitory coinfection is probably needed to create an HIV-stomping, GM superweapon.