# The Vif-APOBEC Nexus

> **NIH NIH R00** · STATE UNIVERSITY NEW YORK STONY BROOK · 2021 · $245,443

## Abstract

The defining hallmark of A3-mediated restriction, explaining genomic plus strand G-to-A mutations in
patient-derived viral sequences. However, the virus deploys a counteraction strategy that utilizes the virus
encoded “virion infectivity factor” (Vif) to polyubiquitinate and degrade the A3s through a cellular
E3-ubiquitin ligase complex. Here, I will use robust and unbiased experimental approaches to 1) identify
separation-of-function Vif mutants that display differential activity against A3D and A3F restriction
enzymes and 2) define the cellular mechanisms that regulate anti-HIV-1 activity of the A3s. My studies will
utilize both hypothesis- and technology-driven approaches and a combination of fundamental virology,
genetics/genome engineering, cell biology, and biochemistry techniques. I anticipate that a better
understanding of the Vif/A3 surfaces and the underlying cellular mechanisms that govern A3 antiviral
activity has the potential to lead to novel strategies to boost the anti-HIV-1 activities of these enzymes and
contribute to the overall NIAID priority of “supporting innovative strategies for treating or curing HIV
infection.”

## Key facts

- **NIH application ID:** 10327772
- **Project number:** 4R00AI147811-03
- **Recipient organization:** STATE UNIVERSITY NEW YORK STONY BROOK
- **Principal Investigator:** Daniel James Salamango
- **Activity code:** R00 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $245,443
- **Award type:** 4N
- **Project period:** 2019-08-06 → 2023-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10327772

## Citation

> US National Institutes of Health, RePORTER application 10327772, The Vif-APOBEC Nexus (4R00AI147811-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10327772. Licensed CC0.

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