HERV-K, or at least the most common types of HERV-K in human cells, appears to be derived from an ancestral beta retrovirus. HERV-W appears to be derived from a gamma retrovirus. So too do HERV-E, HERV-Fc1, HERV-Fc2, HERV-H, HERV-I and HERV-T. A number of these defective proviruses consist of full-length copies with small defects. This means they could likely be resurrected by a helper virus. Chimeric retroviruses are well-known, so these classifications should not be considered hard and fast.
There are active beta retrovirus infections in mice (MMTV), sheep (JSRV) and monkeys (MPMV), and active gamma retrovirus infections in mice (MLV), cats (FLV), pigs (PLV), apes (GALV) and fowl (REV).
REV appears to have evolved and been very active in the 20th century. There is no question that humans are currently exposed to these, but the common assumption that such a virus would breed true in a cellular environment dominated by copies of similar retroviral sequences has not been tested carefully. I've written
a blog post or two on the idea that recombination would quickly convert a similar exogenous retrovirus into something resembling an ERV, which conventional virology would then ignore as harmless. Disease states in which HERV activation is common are well-known, and are not confined to mental illnesses.