Janice E. Clements Ph.D. The Johns Hopkins University School of Medicine 2025 recipient of the ISNV Pioneer in NeuroVirology Award

Dr. Clement’s research focuses on lentiviruses and their role in chronic neurological disease. She developed the first molecular and biochemical tools to study lentivirus molecular biology and was the first to characterize the unusual genome of the lentiviruses. She was also the first scientist to report that HIV is a lentivirus.

As director of the Retrovirus Laboratory, she and her team focus on the molecular virology and pathogenesis of lentivirus infections with emphasis on animal models of AIDS dementia and central nervous system (CNS) disease. Recent discoveries include the use of minocycline, a common antibiotic often used against acne, to protect against viral HIV-related cognitive disease.

Clements has conducted and led research into numerous viruses, concentrating on the animal lentiviruses. Clements was the first to characterize the complex genome of the lentiviruses, describing the genomic structure of visna virus, a lentivirus of sheep. She performed similar work with caprine arthritis encephalitis virus (CAEV), a closely related virus of goats.

With the discovery of AIDS and its cause, HIV, Clements' work took on a new dimension of relevance. In 1985, she published an article with HIV co-discoverer Robert Gallo and others describing the relationship of HIV to visna virus. This article helped to establish HIV as a lentivirus, not a leukemia virus as was originally thought. At the time, the origin of HIV was unknown, and Clements' work presented the possibility that HIV could have been transferred to humans from animals. Later, it was found that simian immunodeficiency virus (SIV) strains from chimpanzee and monkey hosts were the likely progenitors of HIV.

The first SIV macaque model of virus suppression by cART was developed in the Retrovirus Laboratory in collaboration with the Siliciano HIV laboratory. Research projects include studies of viral molecular genetics and host cell genes and proteins involved in the pathogenesis of disease.

Further studies of lentivirus infections and latency of macrophages in the central nervous system and the lung are being pursued to characterize these cells as viral reservoirs during suppressive cART. These studies have led to identify the viral genes that are important in neurovirulence of SIV and the development of CNS disease.

Dr. Clements was the first to identify the role of CD4-independent virus entry in the pathogenesis of neurological disease. They have shown that neurovirulent SIV can infect cells in a CD4-independent, CCR5-dependent manner in primary CNS endothelial cells and cell lines that express only CCR5. Furthermore, studies have shown that the Nef protein from the neurovirulent virus interacts with different cellular kinases than the Nef protein from other strains of SIV. Their studies have demonstrated that replication of neurovirulent virus in vivo by quantitation of viral RNA copies in the brain and viral load in cerebral spinal fluid is directly correlated with the development of CNS lesions during SIV infection.

Finally, they have shown that virus replication in the CNS is independently regulated from the peripheral blood. Because virus replication in the brain is mainly in macrophages, while in the peripheral blood it occurs in lymphocytes, control of viral replication by innate immune responses in the brain is significant. Current research is focused on identifying the mechanism for viral latency in monocytes and macrophages; developing sensitive assays to quantitate latently infected monocytes, macrophages and resting CD4+ T cells in cART suppressed SIV-infected macaques; and identifying approaches to eradicating latently infected cells throughout the body in SIV models to provide a proof of concept for HIV eradication in humans.

Clements and her laboratory have published over 160 scientific articles. Alongside collaborators including Chris Zink, Joseph L. Mankowski, and Kenneth Witwer, Clements has investigated the innate immune response to retrovirus infection in an animal model of HIV encephalitis. Her recent work includes the use of minocycline, a common antibiotic often used against acne, to protect against viral encephalitis and slow viral replication. With Zink, Mankowski and HIV researchers Joel Blankson and Bob Siliciano, Clements has also developed a model of highly active antiretroviral therapy to study viral reservoirs: where HIV conceals itself in the body.

Dr. Clements received her Ph.D. in biochemistry from the University of Maryland. She completed two postdoctoral fellowships at Johns Hopkins—one in molecular biology and virology and the other in neurology. Dr. Clements joined the Johns Hopkins faculty as an assistant professor of neurology in 1979 and then the faculty of the Division of Comparative Medicine in 1988. She was promoted to professor in 1990.