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Joe Watabe, MS
CFAR Developmental Core Manager
Spring 2026 funding cycle: Applications available until Monday, March 2nd, 2pm PT.
- Call opens: Wednesday, January 28, 2026
- Deadline: Monday, March 2, 2026 (2:00 pm PST)
- Funding results: Available before end of June 2026
Amount available: $50,000 in direct costs for 1 year
Apply through the UCSF Resource Allocation Program (RAP) portal
The CFAR Mentored Scientist Award (our primary award program) is a mentoring and training grant targeted toward early stage (either at a senior stage of clinical or postdoctoral training or junior faculty) investigators at UCSF or affiliated partner institutes in the conduct of an HIV research project. These awards are designed to acquire preliminary data and research skills to prepare investigators for a future grant effort. Applicants for this award must indicate a faculty research mentor(s) who will commit to guiding the applicant throughout the duration of the proposed project.
Designation of Mentor
All Mentored award applications from individuals at the Assistant Professor level or below require an HIV research mentor. Mentors can, but are not required to, have supervisory authority over the applicant. CFAR requires your research mentor’s support to advise and guide the research portion of your application before submitting it to RAP.
Of high interest to CFAR are investigations ranging from basic pathogenesis to clinical outcomes in the research areas of HIV/aging and inflammation, latency, cure, vaccines, co-infections, HIV in women, implementation science, and research related to HIV-infected and HIV-impacted Bay Area populations. Projects must be within NIH’s HIV/AIDS research high or medium priority areas. Projects in closely related areas (e.g. TB, HCV, drug use, etc.) must be clearly linked to HIV in order to be eligible for CFAR funding.
The award amount is $50,000 in direct costs for one year.
CFAR requests that applicants review the NIAID HIV Language Guide as they prepare their proposals so that they can follow best practices on language for communicating respectfully about HIV and related topics, including the use of person-first, non-stigmatizing language. Please contact us if you have any questions about this request.
For more detailed information about this RFA, please see the RAP Portal.
To see examples of previously funded projects, see the list below.
Mentored Science Awardees
135 Awards
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Investigating the impact of in utero HIV or malaria exposure on CD4+ T cell development
Investigating the impact of in utero HIV or malaria exposure on CD4+ T cell development
Abstract
Pregnancy-associated malaria, including placental malaria (PM), causes ~100,000 infant deaths per year and maternal HIV infection significantly increases the risk of severe infant morbidity and mortality. Epidemiological studies have reported that children born to mothers with PM have an increased susceptibility to malaria infection. In addition, children born to HIV positive mothers, even those on anti-retroviral therapy (ART), are more prone to severe PM and develop poor vaccine responses.
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Investigating the impact of in utero HIV or malaria exposure on CD4+ T cell development
Investigating the impact of in utero HIV or malaria exposure on CD4+ T cell development
Abstract
Pregnancy-associated malaria, including placental malaria (PM), causes ~100,000 infant deaths per year and maternal HIV infection significantly increases the risk of severe infant morbidity and mortality. Epidemiological studies have reported that children born to mothers with PM have an increased susceptibility to malaria infection. In addition, children born to HIV positive mothers, even those on anti-retroviral therapy (ART), are more prone to severe PM and develop poor vaccine responses.
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Assessing HIV-specific CD8+ T Cell Exhaustion During Antiretroviral Therapy
Assessing HIV-specific CD8+ T Cell Exhaustion During Antiretroviral Therapy
Abstract
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Assessing HIV-specific CD8+ T Cell Exhaustion During Antiretroviral Therapy
Assessing HIV-specific CD8+ T Cell Exhaustion During Antiretroviral Therapy
Abstract
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Does non-pyroptotic IFI16 signaling promote HIV pathogenesis by recruiting new target cells to die?
Does non-pyroptotic IFI16 signaling promote HIV pathogenesis by recruiting new target cells to die?
Abstract
Untreated HIV infection is distinguished by two major clinical hallmarks: progressive depletion of CD4 T cells, and chronic inflammation. We now know that resting “bystander” CD4 T cells in lymphoid tissue undergo a process of abortive HIV infection where incomplete reverse transcripts are formed and detected by the host DNA sensor, interferon gamma-inducible protein 16 (IFI16). This activation of IFI16 causes the assembly of an inflammasome, which cleaves caspase-1 and causes pyroptosis in the CD4 T cell.
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Does non-pyroptotic IFI16 signaling promote HIV pathogenesis by recruiting new target cells to die?
Does non-pyroptotic IFI16 signaling promote HIV pathogenesis by recruiting new target cells to die?
Abstract
Untreated HIV infection is distinguished by two major clinical hallmarks: progressive depletion of CD4 T cells, and chronic inflammation. We now know that resting “bystander” CD4 T cells in lymphoid tissue undergo a process of abortive HIV infection where incomplete reverse transcripts are formed and detected by the host DNA sensor, interferon gamma-inducible protein 16 (IFI16). This activation of IFI16 causes the assembly of an inflammasome, which cleaves caspase-1 and causes pyroptosis in the CD4 T cell.
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Effects of Emtricitabine/tenofovir Disoproxil Fumarate Use on Kidney Health in HIV Pre-exposure Prophylaxis
Effects of Emtricitabine/tenofovir Disoproxil Fumarate Use on Kidney Health in HIV Pre-exposure Prophylaxis
Abstract
Pre-exposure prophylaxis (PrEP) with once-daily oral emtricitabine/tenofovir disoproxil fumarate (FTC/TDF)
prevents acquisition of HIV infection [1-4]. Although well tolerated, [5, 6] cases of nephrotoxicity have occurred
during TDF use, especially in HIV-infected individuals. [7-23] Such cases have resolved in most [7, 22, 24-26] but
not all [15, 19, 23, 27] persons after drug discontinuation, and may involve proximal tubular dysfunction [7-13, 16,
17, 19-22, 24, 26, 28], Fanconi syndrome, [16, 24, 25], or glomerular dysfunction.[7, 10, 11, 14, 15, 21-23, 26, 27]. -
Effects of Emtricitabine/tenofovir Disoproxil Fumarate Use on Kidney Health in HIV Pre-exposure Prophylaxis
Effects of Emtricitabine/tenofovir Disoproxil Fumarate Use on Kidney Health in HIV Pre-exposure Prophylaxis
Abstract
Pre-exposure prophylaxis (PrEP) with once-daily oral emtricitabine/tenofovir disoproxil fumarate (FTC/TDF)
prevents acquisition of HIV infection [1-4]. Although well tolerated, [5, 6] cases of nephrotoxicity have occurred
during TDF use, especially in HIV-infected individuals. [7-23] Such cases have resolved in most [7, 22, 24-26] but
not all [15, 19, 23, 27] persons after drug discontinuation, and may involve proximal tubular dysfunction [7-13, 16,
17, 19-22, 24, 26, 28], Fanconi syndrome, [16, 24, 25], or glomerular dysfunction.[7, 10, 11, 14, 15, 21-23, 26, 27]. -
Determining the Role of TGF-β Signaling in Maintaining HIV Latency in the Gut
Determining the Role of TGF-β Signaling in Maintaining HIV Latency in the Gut
Abstract
Gastrointestinal (GI) tract tissues harbor a large pool of cells latently infected with HIV. However, their exact identity and the mechanisms of latency are unknown. Transforming growth factor (TGF)-β has several functions in gut homeostasis, including the formation and maintenance of tissue-resident memory (TRM) CD8 T cells. Signaling by TGF-β induces expression of CD103, an αE integrin that binds to epithelial E-cadherin. CD4 TRMs also exist, but only a small proportion express CD103, and the role of TGF-β in their formation, function, and maintenance is unknown.
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Determining the Role of TGF-β Signaling in Maintaining HIV Latency in the Gut
Determining the Role of TGF-β Signaling in Maintaining HIV Latency in the Gut
Abstract
Gastrointestinal (GI) tract tissues harbor a large pool of cells latently infected with HIV. However, their exact identity and the mechanisms of latency are unknown. Transforming growth factor (TGF)-β has several functions in gut homeostasis, including the formation and maintenance of tissue-resident memory (TRM) CD8 T cells. Signaling by TGF-β induces expression of CD103, an αE integrin that binds to epithelial E-cadherin. CD4 TRMs also exist, but only a small proportion express CD103, and the role of TGF-β in their formation, function, and maintenance is unknown.