Human Resistance to Feline Leukemia Virus Infection

Humans are routinely exposed to feline leukemia virus (FeLV) through contact with infected cats, but people do not become infected themselves. In a study published in the Journal of Virology, researchers from the University of Glasgow (United Kingdom) and Tulane University (New Orleans) investigated the molecular barriers that protect human cells from FeLV infection.

FeLV is a gammaretrovirus that causes immunosuppression and lymphoma in domestic and wild cats. Although analysis of the human genome shows that humans as a species have been infected with gammaretroviruses in the past, there is no evidence that humans have been infected with FeLV. Other gammaretroviruses are able to jump species, and FeLV may eventually also evolve the ability to infect people, say the authors.

“The potential threat is evident from the human genome sequence, which reveals many past epidemics of gammaretrovirus infection, and from recent cross-species jumps of gammaretroviruses from rodents to primates and marsupials,” the investigators write. Cellular barriers to infection could be crucial in preventing zoonotic transmission of FeLV, they say.

Human serum contains factors that can inactivate retroviruses, but these alone do not appear adequate to prevent FeLV infection, write the authors. To investigate resistance to FeLV infection at the cellular level, they examined the susceptibility of various human cell types to FeLV-B, the variant most likely to be capable of infecting humans.

The researchers found that some human cell types were more resistant than others to FeLV-B infection. Keratinocytes, lung fibroblasts, and a range of cancer-derived cell lines were fully or partially permissive—that is, they allowed viral replication within the cell. Hematopoietic cells in general were less permissive, and peripheral blood mononuclear cells in particular were nonpermissive for viral replication.

All human cell lines were susceptible to initial infection with FeLV-B. In less permissive cell types, however, cellular enzymes induced gene mutations within the virus, blocking its replication. Peripheral blood mononuclear cells blocked the virus without causing mutations, suggesting that factors within these cells prevented the expression of viral genes. “Since cells derived from other normal human cell types are fully supportive of FeLV replication, innate resistance of blood cells could be critical in protecting against cross-species infection,” write the authors.

“Can the risk of zoonotic infection with FeLV be discounted?” they ask. Primate lentiviruses (another genus of retrovirus) have been able to cross species even though cellular protections against these viruses appear to be more numerous than the barriers to FeLV infection. The authors conclude that “future adaptation of FeLV for zoonotic spread is not beyond the repertoire of this virus family.”

Dr. Laurie Anne Walden received her doctorate in veterinary medicine from North Carolina State University. After an internship in small animal medicine and surgery at Auburn University, she returned to North Carolina, where she has been in small animal primary care practice for over 20 years. Dr. Walden is also a board-certified editor in the life sciences and owner of Walden Medical Writing, LLC. She works as a full-time freelance medical writer and editor and continues to see patients a few days each month.