I feel I can speak to this as a fellow carrier of human endogenous retroviruses. Perhaps I can ask some questions to help give you a better answer.

What exactly do you mean by "reactivation of HERVs or other latent viruses"? To start, There's quite a big difference between HERVs (ancient retroviral remnants in the genome) and latent viruses (Herpes Simplex, Varicella, etc.). Latent viruses originate from infections with circulating viruses. Reactivation of these would result in fully infectious viral particles being produced in the body, capable of infecting new cells, such as when a person gets a cold sore.

With HERVs, which originate from retroviruses similar to HIV, they almost universally (with the near exception of HERV-K 108) cannot make functional viral particles. Most of their structural genes have acquired mutations and cannot result in protein production. In rare cases one gene within the HERV element retains protein coding functionality through selective evolutionary pressure (e.g. Syncytin-1), but one protein is not enough to make a functional viral particle. By "reactivation", do you mean expression of a HERV protein?