In our findings, the viral interaction in HIV/EBV-1 coinfection may have occurred through a proinflammatory pathway due to the correlation of HIV viral load with IL-6 and IFN-γ, potentially resulting in the plausible depletion of helper T lymphocytes, which is a well-known profile for the attempted control and suppression of the most evident infection in the early stages of the disease [50]. This evidence concerns the gene IL6 and coinfection.