# LDH VIRUS: GROWTH IN MACROPHAGES & PERSISTENT INFECTION

> **NIH NIH R01** · UNIVERSITY OF MINNESOTA · 1988 · $114,990

## Abstract

The lactate dehydrogenase-elevating virus (LDV) possesses a
number of unique properties which makes it an ideal model system
for studying mechanisms of virus persistence and induction of
paralytic disease by a virus that normally causes only a benign
infection.  LDV replicates only in a subpopulation of macrophages
in the mouse.  Upon primary infection, these cells seem to
succumb to productive infection resulting in extensive viremia,
transient production of interferon, and elevation of certain
enzymes in the blood.  This acute infection invariably progresses
into a life long, persistent infection associated with low virus
production and an immune response to the virus.  The persistence
seems to be maintained by the continuous transfer of the virus to
newly formed permissive macrophages.  A poor neutralizing
capacity of mouse antibody, immune enhancement of infectivity
and the development of antigenic variants may be factors
contributing to persistence.  Infection of most mouse strains does
not result in clinical disease.  The exception are C58 and AKR
mice in which an acute infection induces a rapid and fatal
polioencephalomyelitis provided the mice have passed a certain
age and are immunosuppressed.  Our main goal at present is to
sequence the entire genome of LDV.  cDNA has been cloned in
pUC19 (clones range from 50 to 2500 bp), subcloned into M13
bacteriophage and is being sequenced by the dideoxynucleodite
chain termination method.  Such sequence data will be very
valuable in combination with monoclonal antibodies, which are
presently being isolated in future studies of the molecular basis of
antigenic variants of LDV and variants differing in
neurovirulence, of the epitopes of the LDV glycoprotein
interacting with neutralizing antibodies and of the nature and
function of the nonstructural proteins of LDV, which potentially
account for 90% of the coding capacity of the genome.  In
addition, we plan to identify the cells in the mouse that support
LDV replication during the acute and persistent phases of
infection by combined in situ hybridization and
immunocytochemistry of tissue and whole body sections.  The
sections will be sequentially incubated with biotinylated mouse
anti-LDV IgG, avidine-peroxidase complex and peroxidase
substrate and then hybridized with 125I-labeled cDNA probes.  We
will also attempt to develop a cell culture line permissive for LDV
replication for further biochemical studies of LDV replication and
the in vitro titration of infectious LDV.

## Key facts

- **NIH application ID:** 3126119
- **Project number:** 5R01AI015267-18
- **Recipient organization:** UNIVERSITY OF MINNESOTA
- **SAM.gov UEI:** KABJZBBJ4B54
- **Principal Investigator:** PETER G PLAGEMANN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $114,990
- **Award type:** 5
- **Project period:** 1978-07-01 → 1991-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3126119

## Citation

> US National Institutes of Health, RePORTER application 3126119, LDH VIRUS: GROWTH IN MACROPHAGES & PERSISTENT INFECTION (5R01AI015267-18). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3126119. Licensed CC0.

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