# IMMUNITY AND VIRUS DISEASE

> **NIH NIH R01** · UNIV OF MASSACHUSETTS MED SCH WORCESTER · 1987 · $186,448

## Abstract

The role of natural killer(NK) and other natural cytotoxic effector cells
in regulating virus infections will be examined.  Model systems will be
mice infected with mouse cytomegalovirus(MCMV), lymphocytic
choriomeningitis virus(LCMV), and mouse hepatitis virus(MHV).  Using
microcytotoxicity assays and leukocyte fractionation schemes, the effector
cells mediating "natural" cytotoxicity against virus-infected cultured
cells will be identified under conditions that discriminate between NK
cells, natural cytotoxic(NC) cells, a newly described virus-killer(VK)
cell, and cytotoxic macrophages.  Similarly, cytotoxicity in vivo will be
examined by injecting mice intravenously and by other routes with 125
iododeoxyuridine-labeled virus-infected cells and determining the loss of
radioactivity in vivo.  Leukocytes will be transferred into such mice after
immunosuppression to identify the effector system mediating the
cytotoxicity.  A major technique to distinguish NK mechanisms from other
mechanisms in this and other systems will be to inject mice (or treat
leukocytes in culture) with antibody to asialo GM1, which selectively
depletes NK cell activity while leaving other known effector systems
intact.  Using this and other immune reagents, the effects of NK cells on
virus titers, pathology, mortality, and immunosuppression during acute and
persistent virus infections in vivo will be delineated.  The progression of
MCMV, LCMV, and MHV in NK cell-depleted mice will be examined, and attempts
will be made to reconstitute their resistance by transfer of purified NK
cells and NK clones.  The effects of NK cells under conditions of
interferon or antiviral antibody treatment will be similarly examined in
virus-infected mice.  The possibility that virus-infected cells may
chemotactically attract NK cells will also be tested.  Our recent data
indicate that natural cytotoxic cells may play major roles in limiting
virus infections, but several effector systems may be involved, and
different systems may vary in importance with injection route and target
organ.  Understanding such cytotoxic mechanisms would be of use in
preventing or limiting virus infections in man.

## Key facts

- **NIH application ID:** 3127365
- **Project number:** 5R01AI017672-08
- **Recipient organization:** UNIV OF MASSACHUSETTS MED SCH WORCESTER
- **SAM.gov UEI:** MQE2JHHJW9Q8
- **Principal Investigator:** Raymond M Welsh
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $186,448
- **Award type:** 5
- **Project period:** 1980-07-01 → 1989-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3127365

## Citation

> US National Institutes of Health, RePORTER application 3127365, IMMUNITY AND VIRUS DISEASE (5R01AI017672-08). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3127365. Licensed CC0.

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