# Antibody-Based Enhancement of CMV Vaccine Vectors for HIV

> **NIH NIH K01** · OREGON HEALTH & SCIENCE UNIVERSITY · 2020 · $100,000

## Abstract

PROJECT SUMMARY
Over 36 million people are living with human immunodeficiency virus (HIV) and it infects over 1 million new
people every year. Several advancements in treatment and prevention have helped reduce HIV incidence and
AIDS-related deaths, but are insufficient to stem the spread of the epidemic. An effective HIV vaccine is needed
to help reduce new HIV infections. As demonstrated by the RV144 Thai Vaccine Trail, a successful HIV vaccine
will need to induce both antibodies to prevent acquisition and a cellular immune response to control breakthrough
virus. Rhesus cytomegalovirus, strain 68-1, expressing SIV antigens (RhCMV/SIV) enables stringent control of
SIV replication in 50% of vaccinated rhesus macaques. This vaccine protects animals by inducing effector
memory T cells that reside at the portals of entry. While the CD8+ T cell response in vaccinated rhesus macaques
is well-characterized and highly unconventional, it does not directly correlate with protection. In contrast, little is
known about the RhCMV/SIV-induced CD4+ T cell response. Because the rhesus macaque is outbred and
diverse, their MHC II alleles are complex and prevent controlled studies of the CD4+ T cell response. In contrast,
Mauritian cynomolgus macaques have limited genetic diversity and we can identify MHC-II-matched MCM.
Therefore, we will vaccinate MHC-II-matched MCM with CyCMV expressing SHIV antigens to study the CD4+ T
cell response. We predict that the frequency and function of the SHIV-specific CD4+ T cell response will correlate
with post-infection SHIV control. In addition, CMV vaccine vectors for HIV do not protect against acquisition and
do not elicit neutralizing antibodies. Therefore, we intend to induce antibodies in conjunction with CyCMV
vaccination by combining CyCMV with sequential HIV-Env DNA/protein immunizations. We hypothesize that
CMV vaccine regimens can be enhanced to protect against acquisition by the induction of HIV-Env specific
antibodies and can protect against a novel SHIV challenge virus. In conclusion, we propose to enhance our
understanding of CMV vaccine vectors and to increase the protective efficacy of this vaccine regimen. These
findings will be directly applicable to impending clinical trials of CMV vaccine vectors in humans for HIV.

## Key facts

- **NIH application ID:** 10133318
- **Project number:** 3K01OD026561-03S1
- **Recipient organization:** OREGON HEALTH & SCIENCE UNIVERSITY
- **Principal Investigator:** Justin Greene
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $100,000
- **Award type:** 3
- **Project period:** 2018-09-01 → 2020-11-01

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10133318

## Citation

> US National Institutes of Health, RePORTER application 10133318, Antibody-Based Enhancement of CMV Vaccine Vectors for HIV (3K01OD026561-03S1). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10133318. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*