J. Ellard's research while affiliated with La Trobe University and other places
What is this page?
This page lists the scientific contributions of an author, who either does not have a ResearchGate profile, or has not yet added these contributions to their profile.
It was automatically created by ResearchGate to create a record of this author's body of work. We create such pages to advance our goal of creating and maintaining the most comprehensive scientific repository possible. In doing so, we process publicly available (personal) data relating to the author as a member of the scientific community.
If you're a ResearchGate member, you can follow this page to keep up with this author's work.
If you are this author, and you don't want us to display this page anymore, please let us know.
It was automatically created by ResearchGate to create a record of this author's body of work. We create such pages to advance our goal of creating and maintaining the most comprehensive scientific repository possible. In doing so, we process publicly available (personal) data relating to the author as a member of the scientific community.
If you're a ResearchGate member, you can follow this page to keep up with this author's work.
If you are this author, and you don't want us to display this page anymore, please let us know.
Publications (2)
Objective:
Human papillomavirus (HPV)-related anal cancer rates are increasing and are particularly high in gay, bisexual and other men who have sex with men (GBM/MSM), especially HIV-positive individuals. Although screening programs for high-risk populations have been advocated, concerns about possible adverse psychological consequences exist. Th...
Background. Most anal cancers are attributable to persistent human papillomavirus type 16 (HPV-16) infection. The anal cancer precursor, high-grade squamous intraepithelial lesion (HSIL), frequently regresses spontaneously. We hypothesized that T-cell responses are associated with HSIL regression.
Methods. In men who have sex with men undergoing an...
Citations
... HPV subtypes differ in their genetic sequence and are categorized as low-risk or high-risk based on their oncogenic potential (4)(5)(6). Additionally, 14 HPV types are designated as human carcinogenic, including high-risk HPV (HR-HPV; HPV16, 18,31,33,35,39,45,51,52,56,58,59, and 68) (7,8). High-risk HPV strains, predominantly 16 and 18, are responsible for almost all cervical cancer cases. ...
... Of particular importance may be the persistent depletion of CD4 + T cells from the mucosal compartments in PWH who have been treated during chronic infection (11,12), which may create a more favorable microenvironment for precancerous lesions to develop and progress. In this sense, altered cell-mediated immunity has been associated with increased HPV infection and disease (13), while immune responses orchestrate regression of HPV-related lesions (14). ...