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1: J Virol. 1993 Sep;67(9):5383-93.  Related Articles, Links  


Evidence for a novel regulatory pathway for herpes simplex virus gene
expression in trigeminal ganglion neurons.

Kosz-Vnenchak M, Jacobson J, Coen DM, Knipe DM.

Department of Microbiology and Molecular Genetics, Harvard Medical
School, Boston, Massachusetts 02115.

Thymidine kinase (TK)-negative (TK-) mutant strains of herpes simplex
virus type 1 (HSV-1) show reduced expression of alpha and beta viral
genes during acute infection of trigeminal ganglion neurons following
corneal infection (M. Kosz-Vnenchak, D. M. Coen, and D. M. Knipe, J.
Virol. 64:5396-5402, 1990). It was surprising that a defect in a beta
gene product would lead to decreased alpha and beta gene expression,
given the regulatory pathways demonstrated for HSV infection of
cultured cells. In this study, we have examined viral gene expression
during reactivation from latent infection in explanted trigeminal
ganglion tissue. In explant reactivation studies with wild-type virus,
we observed viral productive gene expression over the first 48 h of
explant incubation occurring in a temporal order (alpha, beta, gamma)
similar to that in cultured cells. This occurred predominantly in
latency-associated transcript-positive neurons but was limited to a
fraction of these cells. In contrast, TK- mutant viruses showed
greatly reduced alpha and beta gene expression upon explant of
latently infected trigeminal ganglion tissue. An inhibitor of viral TK
or an inhibitor of viral DNA polymerase greatly decreased viral lytic
gene expression in trigeminal ganglion tissue latently infected with
wild-type virus and explanted in culture. These results indicate that
the regulatory mechanisms governing HSV gene expression are different
in trigeminal ganglion neurons and cultured cells. We present a new
model for viral gene expression in trigeminal ganglion neurons with
implications for the nature of the decision process between latent
infection and productive infection by HSV.

PMID: 8394454 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

2: J Virol. 1990 Nov;64(11):5396-402.  Related Articles, Links  


Restricted expression of herpes simplex virus lytic genes during
establishment of latent infection by thymidine kinase-negative mutant
viruses.

Kosz-Vnenchak M, Coen DM, Knipe DM.

Department of Microbiology, Harvard Medical School, Boston,
Massachusetts 02115.

Infection of cells by herpes simplex virus (HSV) can lead to either
lytic, productive infection or nonlytic, latent infection. The factors
influencing this infection pathway decision are largely unknown.
Thymidine kinase-negative mutant viruses can establish latent
infection in neurons of mouse trigeminal ganglia but do not replicate
productively in these cells. We show that during the early stages of
establishment of latency by these mutants, expression of viral lytic
genes is drastically reduced or undetectable as assayed by in situ
hybridization. Thus, establishment of latent infection by HSV can
occur despite severely restricted levels of lytic gene expression.
This suggests that the block to productive replication during
establishment of latent infection by HSV occurs before or early during
the expression of alpha genes.

PMID: 2170678 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

3: J Gen Virol. 1991 Mar;72 ( Pt 3):641-9.  Related Articles, Links  

Investigation of herpes simplex virus type 1 (HSV-1) gene expression
and DNA synthesis during the establishment of latent infection by an
HSV-1 mutant, in1814, that does not replicate in mouse trigeminal
ganglia.

Valyi-Nagy T, Deshmane SL, Spivack JG, Steiner I, Ace CI, Preston CM,
Fraser NW.

Wistar Institute, Philadelphia, Pennsylvania 19104.

In previous studies, the herpes simplex virus type 1 (HSV-1) mutant,
in1814, which lacks the trans-inducing function of Vmw65, did not
replicate in the trigeminal ganglia of mice following corneal
inoculation but did establish a reactivatable latent infection in the
ganglia 12 to 24 h after ocular infection. Since in1814 did not
replicate in vivo, the molecular events during the establishment phase
of latent HSV-1 infection could be characterized without the
complications of concurrent productive viral infection. In comparison
to parental HSV-1 strain 17+, the expression of viral immediate early
(IE), early and late genes and the levels of viral DNA in the
trigeminal ganglia of mice following in1814 infection were greatly
reduced. However, accumulation of latency-associated transcripts, a
prominent feature of latent HSV-1 infection, occurred in a wild-type
fashion. Furthermore, low levels of viral gene expression and an
increase in the level of viral DNA in the in1814-infected ganglia were
not detected until 1 to 2 days after the establishment of HSV-1
latency. Thus, IE gene expression and replication of viral DNA in the
trigeminal ganglia are not prerequisites for the establishment of
HSV-1 latency. These results suggest that the pathways leading to
productive and latent infections in neurons may diverge at an early
stage of the host-HSV-1 interaction and that the level of viral IE
gene expression has a key role in determining the outcome of
infection.

PMID: 1848599 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

4: Virology. 1992 Mar;187(1):348-52.  Related Articles, Links  

Replication, latent infection, and reactivation in neuronal culture
with a herpes simplex virus thymidine kinase-negative mutant.

Wilcox CL, Crnic LS, Pizer LI.

Department of Microbiology, University of Colorado School of Medicine,
Denver 80262.

Herpes simplex virus type 1 (HSV-1) mutant viruses lacking functional
viral thymidine kinase activity are reported to be incapable of
replication in neurons. To investigate the role of viral thymidine
kinase (TK) activity in the HSV-1 infection of the neuron, we studied
a thymidine kinase-negative (TK-) mutant virus engineered to eliminate
TK function without affecting the other known transcripts encoded in
this region of the genome. Studies using the mouse eye model
demonstrated that the mutant behaved as is reported for other TK-
viruses: DNA of the mutant virus was detected in the ganglia during
the latent infection by polymerase chain reaction, but virus did not
reactivate after explantation of the ganglia. Utilizing the neuronal
cultures, we investigated the ability of the mutant virus to replicate
in neurons and the capacity of the mutant virus to establish latency
and reactivate. With a low multiplicity of infection (m.o.i.),
replication of the TK- mutant virus in sensory neurons in culture was
significantly delayed compared to that of the wild-type virus.
However, when a high m.o.i. was used, the mutant and the wild-type
viruses replicated with similar kinetics. The TK- mutant virus was
capable of establishment of latency and reactivation from the latent
infection in sensory neurons in culture. These data suggest that HSV-1
thymidine kinase activity facilitates viral replication, but that TK
activity is not essential for either replication or reactivation from
latent infections in neurons in vitro.

PMID: 1310559 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

5: J Virol. 1987 Jul;61(7):2171-4.  Related Articles, Links  


Trigeminal ganglion infection by thymidine kinase-negative mutants of
herpes simplex virus after in vivo complementation.

Tenser RB, Edris WA.

Infection of trigeminal ganglion by herpes simplex virus (HSV)
thymidine kinase-negative (TK-) mutants was investigated in mixed
infection studies in mice. Mice were corneally inoculated with TK- HSV
alone or with mixtures of TK- HSV-TK+ HSV. When inoculated alone, an
arabinosylthymine-selected HSV type 1 TK- mutant and a HSV type 2 TK-
deletion mutant infected mouse ocular tissues but rarely infected
ganglion tissues. However, both TK- mutants readily infected ganglion
tissues when they were inoculated in mixtures with TK+ HSV. By means
of mixed infection studies, it was demonstrated that TK- HSV could
readily establish acute and latent ganglion infections. It was thought
that the frequent infection of trigeminal ganglion tissue by both TK-
mutants after mixed TK(-)-TK+ HSV infection was the result of in vivo
complementation. After mixed TK(-)-TK+ HSV infection and subsequent
cultivation of ganglion explants in arabinosylthymine, results
supported the conclusion that when TK- was present in ganglia it was
in the same neurons that contained TK+ HSV.

PMID: 3035217 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

6: J Virol. 1988 May;62(5):1479-85.  Related Articles, Links  


Expression of herpes simplex virus type 1 latency-associated
transcripts in the trigeminal ganglia of mice during acute infection
and reactivation of latent infection.

Spivack JG, Fraser NW.

Wistar Institute, Philadelphia, Pennsylvania 19104.

Herpes simplex virus type 1 (HSV-1) establishes a latent infection in
the trigeminal ganglia of mice infected via the eye. In these ganglia
three viral transcripts, of 2.0, 1.5, and 1.45 kilobases (kb), which
are at least partially colinear, have been identified by Northern
(RNA) blot analysis. These RNAs partially overlap ICPO, but are
transcribed in the opposite direction (J. G. Spivack and N. W. Fraser,
J. Virol. 61:3841-3847, 1987). The accumulation of these
latency-associated transcripts, as well as other viral RNAs, was
studied during an acute infection and the reactivation of a latent
HSV-1 infection in mice. The 2.0-kb latency-associated transcript was
detected in trigeminal ganglia of mice as early as 4 days
postinfection, and the 1.45- and 1.5-kb RNA doublet was detected at 14
days postinfection. The levels of these latency-associated transcripts
increased steadily over a 60-day period. In contrast, other HSV-1
transcripts were detected at 2 to 3 days postinfection, reached a peak
on day 4, and rapidly declined below detectable levels by day 7. The
data indicate that the temporal expression of the latency-associated
genes during acute infection in the trigeminal ganglia of mice is
different from the temporal expression of genes involved in HSV-1
replication. During the reactivation of latent HSV-1 from explanted
trigeminal ganglia, the latency-associated RNAs decreased about
twofold, but were present at significant levels even after HSV-1 DNA
increased and infectious virus was recovered. The decrease of the
latency-associated transcripts occurred when reactivation was blocked
by phosphonoacetic acid or novobiocin, which suggests that this
decrease may be an early event in the entry of latent HSV-1 into the
viral replication cycle.

PMID: 2833602 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

7: Ann Neurol. 1982 Mar;11(3):285-91.  Related Articles, Links  

Detection of herpes simplex virus mRNA in latently infected trigeminal
ganglion neurons by in situ hybridization.

Tenser RB, Dawson M, Ressel SJ, Dunstan ME.

Latent infection of the trigeminal ganglion with herpes simplex virus
type 2 (HSV-2) was studied in guinea pigs by in situ DNA
hybridization. Frozen ganglion sections from animals killed during the
period of latent virus infection were studied under nondenaturing
conditions. Some sections were treated with deoxyribonuclease (DNase)
or ribonuclease (RNase) before incubation with HSV DNA probes. HSV
probes consisted of viral DNA nick translated and labeled in vitro
with tritiated nucleotides. Bacteriophage lambda DNA, similarly
prepared, was used as a control probe. The lambda probe was negative
in all situations, including HSV-2-infected monolayer cells in cell
culture. HSV-2 probes produced heavy label and, therefore, evidence of
hybridization with HSV-2-infected monolayer cells. When HSV-2 probes
were incubated with latently infected ganglion sections, hybridization
was detected in 71% of guinea pigs and 46% of ganglia. Label was seen
only in neurons, and in positive ganglia 0.3 to 5% of neurons were
labeled. The amount of label was markedly decreased by pretreatment of
ganglion sections with RNase but not DNase, indicating that the DNA
probes hybridized to HSV messenger RNA in the latently infected
ganglia.

PMID: 6284019 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

8: J Virol. 1997 Aug;71(8):5885-93.  Related Articles, Links  

 
A LAT-associated function reduces productive-cycle gene expression
during acute infection of murine sensory neurons with herpes simplex
virus type 1.

Garber DA, Schaffer PA, Knipe DM.

Department of Microbiology and Molecular Genetics, Harvard Medical
School, Boston, Massachusetts 02115, USA.

Herpes simplex virus (HSV) persists in the human population by
establishing long-term latent infections followed by periodic
reactivation and transmission. Latent infection of sensory neurons is
characterized by repression of viral productive-cycle gene expression,
with abundant transcription limited to a single locus that encodes the
latency-associated transcripts (LATs). We have observed that LAT-
deletion mutant viruses express viral productive-cycle genes in
greater numbers of murine trigeminal ganglion neurons than LAT+ HSV
type 1 at early times during acute infection but show reduced
reactivation from latent infection. Thus, a viral function associated
with the LAT region exerts an effect at an early stage of neuronal
infection to reduce productive-cycle viral gene expression. These
results provide the first evidence that the virus plays an active role
in down-regulating productive infection during acute infection of
sensory neurons. The effect of down-regulation of productive-cycle
gene expression during acute infection may contribute to viral evasion
from the host immune responses and to reduced cytopathic effects,
thereby facilitating neuronal survival and the establishment of
latency.

PMID: 9223478 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

9: Intervirology. 1991;32(2):76-92.  Related Articles, Links  

Role of herpes simplex virus thymidine kinase expression in viral
pathogenesis and latency.

Tenser RB.

Department of Medicine (Neurology), Pennsylvania State University
College of Medicine, Hershey 17033.

Herpes simplex virus (HSV) thymidine kinase (TK) expression and the
HSV TK gene have been evaluated in studies of gene control, as well as
in animal and human studies of viral pathogenesis, including HSV
latency. In investigations of the biological role of HSV TK, enzyme
expression was noted to be important for HSV infection of
nonreplicating cells in culture; and, in experimental animal studies,
HSV TK was shown to be important for in vivo latent infection of
sensory ganglion neurons. Latency in these studies was determined by
the ability of HSV to reactivate from sensory ganglion explants. In
recent studies, investigators sought to determine whether the role HSV
TK expression plays in latency is primarily in the establishment and
maintenance of latency or in the reactivation process. Following
infection of experimental animals with HSV TK-deficient mutants, the
presence of HSV in ganglia was detected in complementation, rescue,
and molecular biological studies. Results suggest that HSV TK
expression may be important for HSV reactivation from latency. This
was supported by in situ hybridization investigations. In the latter
studies, HSV latency associated transcript (LAT) was present in
ganglion neurons, although reactivation of HSV from such ganglia was
defective. LAT-expressing, reactivation-defective infections
established by TK mutants of HSV are considered examples of incomplete
latency. From the present review, it appears that HSV TK expression,
particularly TK expression of HSV-1, is important for the reactivation
of latent HSV infection of sensory ganglion neurons, probably because
of limited neuronal TK expression and absent replication capacity of
these cells.

Publication Types:
Review
Review, Academic

PMID: 1851146 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

10: J Virol. 1990 Nov;64(11):5342-8.  Related Articles, Links  


Characterization of herpes simplex virus type 2 transcription during
latent infection of mouse trigeminal ganglia.

Mitchell WJ, Deshmane SL, Dolan A, McGeoch DJ, Fraser NW.

Wistar Institute, Philadelphia, Pennsylvania 19104-4268.

Using a cornea trigeminal ganglion model, we have investigated
transcription by herpes simplex virus type 2 (HSV-2) during latency in
mice. Latency was verified 2 months postinoculation by reactivation of
HSV-2 after explant cocultivation of trigeminal ganglia from the
majority of mice (83%). Transcription during latent HSV-2 infection
was limited to the repeat regions of the viral genome as determined by
in situ hybridization using restriction fragment probes representing
100% of the HSV-2 genome. Further mapping of the positively
hybridizing region by using subfragments showed that transcription
occurred from approximately 11.5 kb of contiguous DNA fragments. A
1.0-kb PvuI-BamHI fragment within the BamHI F fragment and a 0.3-kb
BamHI-SalI fragment and a 3.4-kb SalI-BamHI fragment within the BamHI
P fragment hybridized more strongly than other subfragments in in situ
hybridization experiments. All positive signals were confined to the
nucleus. The RNA that hybridized to the 3.4-kb SalI-BamHI DNA fragment
probe by in situ hybridization corresponded to a 2.3-kb transcript on
Northern (RNA) blots. Under our conditions for Northern blot
hybridization, the 3.4-kb SalI-BamHI probe of HSV-2 hybridized to a
limited degree with the latency-associated transcripts of HSV-1.
Shorter spliced species of latency-associated transcript RNA, which
are seen during HSV-1 latency, have not been detected in latent HSV-2
RNA. However, viral gene expression during HSV-2 latency appears to be
very similar to that during HSV-1 latency.

PMID: 2170675 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

11: Virology. 1988 Nov;167(1):279-83.  Related Articles, Links  

Beta-galactosidase as a marker in the peripheral and neural tissues of
the herpes simplex virus-infected mouse.

Ho DY, Mocarski ES.

Department of Medical Microbiology, Stanford University School of
Medicine, California 94305.

We have inserted a modified Escherichia coli lacZ gene, placed under
the control of herpes simplex virus alpha 4 or beta 8 regulatory
signals, into the HSV-1 genome disrupting the viral thymidine kinase
gene. Using beta-galactosidase as an in situ indicator of viral gene
expression, we detected expression from these recombinant HSV in
dermal and neural tissues of the BALB/c mouse. Our detection of
beta-galactosidase expression in neuronal cells indicates that
TK-deficient viruses are capable of invading mouse neuronal cells and
expressing up to the beta class of gene product.

PMID: 2847416 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

12: J Virol. 1993 Nov;67(11):6903-8.  Related Articles, Links  


Herpes simplex virus thymidine kinase and specific stages of latency
in murine trigeminal ganglia.

Jacobson JG, Ruffner KL, Kosz-Vnenchak M, Hwang CB, Wobbe KK, Knipe
DM, Coen DM.

Department of Biological Chemistry and Molecular Pharmacology, Harvard
Medical School, Boston, Massachusetts 02115.

From marker rescue, sequencing, transcript, and latency analyses of
the thymidine kinase-negative herpes simplex virus mutant dlsactk and
studies using the thymidine kinase inhibitor Ro 31-5140, we infer that
the virus-encoded thymidine kinase is required in murine trigeminal
ganglia for acute replication and lytic gene expression, for
increasing the numbers of cells expressing latency-associated
transcripts, and for reactivation from latent infection.

PMID: 8411396 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

13: J Virol. 1988 Mar;62(3):749-56.  Related Articles, Links  


Latent herpes simplex virus type 1 transcripts in peripheral and
central nervous system tissues of mice map to similar regions of the
viral genome.

Deatly AM, Spivack JG, Lavi E, O'Boyle DR 2nd, Fraser NW.

Wistar Institute, Philadelphia, Pennsylvania 19104-4268.

Herpes simplex virus type 1 (HSV-1) DNA and RNA have been detected in
peripheral nervous system (PNS) and central nervous system (CNS)
tissues of latently infected mice. However, explant methods are
successful in reactivating HSV-1 only from latently infected PNS
tissues. In this report, latent herpesvirus infections in mouse PNS
and CNS tissues were compared by in situ hybridization to determine
whether the difference in reactivation was at the level of the virus
or the host tissue. It was demonstrated that the HSV-1 transcripts
present during latency in the mouse PNS and CNS originated from the
same region of the genome, the repeats which bracket the long unique
sequence. Therefore, the difference in reactivation with PNS and CNS
tissues cannot be accounted for by differences in the extent of the
HSV-1 genome transcribed during herpesvirus latency. Latent HSV-1 RNA
was detected in the trigeminal ganglia (PNS) and the trigeminal system
in the CNS from the mesencephalon to the spinal cord as well as other
regions of the CNS not noted previously. Latent HSV-1 RNA was found
predominantly in neurons but also in a small number of cells which
could not be identified as neuronal cells. It is suggested that host
differences in CNS and PNS tissues, rather than differences in latent
virus transcription, may be important determinants in the HSV-1
reactivation process in explanted tissues.

PMID: 2828670 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

14: Proc Natl Acad Sci U S A. 1989 Oct;86(19):7596-600.  Related
Articles, Links


Herpes simplex virus latent RNA (LAT) is not required for latent
infection in the mouse.

Ho DY, Mocarski ES.

Department of Microbiology and Immunology, Stanford University School
of Medicine, CA 94305.

During latent infection by herpes simplex virus (HSV), an abundant
latency-associated transcript (LAT) that is antisense to a predominant
viral alpha gene (ICP0) is found localized in the nucleus of sensory
neurons. We disrupted both copies of the LAT gene in the HSV-1 genome
by insertion of the Escherichia coli lacZ gene under LAT promoter
control. The resulting recombinant virus, RH142, does not express any
detectable LAT in either latently or productively infected cells,
although beta-galactosidase expression is readily detectable in
sensory neurons of latently infected mice. Expression was first
detectable 3 days postinoculation and continued at approximately the
same level for the entire experimental period (56 days).
beta-Galactosidase expression was not detectable at any time during
RH142 replication in Vero cells. Thus, the kinetics of expression and
cell-type specificity of the LAT gene are distinct from other HSV-1
genes that are expressed during productive growth. When latently
infected trigeminal ganglia were explanted, RH142 reactivated from
latency with the kinetics and an efficiency indistinguishable from the
parental wild-type virus. These studies argue against any possible
antisense regulatory mechanism of LAT in the regulation of viral gene
expression or any role of LAT-encoded protein during the establishment
or maintenance of latency in the mouse.

PMID: 2552449 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

15: J Virol. 1989 Jun;63(6):2861-5.  Related Articles, Links  


Latency-associated transcript but not reactivatable virus is present
in sensory ganglion neurons after inoculation of thymidine
kinase-negative mutants of herpes simplex virus type 1.

Tenser RB, Hay KA, Edris WA.

Department of Medicine (Neurology), Pennsylvania State University
College of Medicine, Hershey 17033.

The presence of herpes simplex virus (HSV) latency-associated
transcript (LAT) was investigated in sensory ganglion neurons of mice
after inoculation with thymidine kinase (TK) mutants of HSV. Ganglion
serial sections were examined in order to quantitate numbers of
LAT-positive neurons. After inoculation with TK-positive HSV, virus
was isolated during latency from explants of most ganglia, and LAT was
detected by in situ hybridization in 96% of ganglia. After inoculation
with HSV TK mutants, virus was isolated from 0% of ganglia, but LAT
was detected in 95 to 100% of ganglia. After inoculation of TK mutants
of HSV, therefore, although latent infection as indicated by the
isolation of virus from ganglion explants was not detected, the
presence of LAT was common. These results suggest that the lack of
reactivatable virus after inoculation of HSV TK mutants may be related
to a role for HSV TK expression in the reactivation process.

PMID: 2542595 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

16: J Virol. 1991 Aug;65(8):4142-52.  Related Articles, Links  


Induction of cellular transcription factors in trigeminal ganglia of
mice by corneal scarification, herpes simplex virus type 1 infection,
and explantation of trigeminal ganglia.

Valyi-Nagy T, Deshmane S, Dillner A, Fraser NW.

Wistar Institute, Philadelphia, Pennsylvania 19104-4268.

In a mouse model for herpes simplex virus type 1 (HSV-1) latency in
which the virus was inoculated via the eye after corneal
scarification, HSV-1 replicated in corneal epithelial cells and
infected the nerve cell endings. HSV-1 reached the trigeminal ganglia
by fast axonal transport between 2 and 10 days postinfection (p.i.)
and established a latent infection in neuronal cells or replicated and
spread to nonneuronal cells. By using in situ hybridization, we showed
that cellular transcription factors are stimulated by HSV-1 infection
in trigeminal ganglia. This stimulation is biphasic, peaking at 1 and
3 to 4 days p.i. The first peak involves c-jun and oct-1 expression in
neurons, and the second involves c-jun, c-fos, and oct-1 expression in
neurons and nonneuronal cells. Corneal scarification, alone or
followed by infection with UV-inactivated HSV-1, induced monophasic
c-jun and oct-1 expression in some neurons of the trigeminal ganglia,
with a peak at 1 day p.i. Corneal infection without prior
scarification induced c-jun, c-fos, and oct-1 expression in some
neuronal and nonneuronal cells of the trigeminal ganglia 2 to 9 days
p.i. Explanation of ganglia from latently infected animals resulted in
reactivation of the latent virus. Independently of the presence of
latent HSV-1 in explanted ganglia, expression of c-fos, c-jun, and
oct-1 was induced first in nonneuronal cells, peaking 6 to 10 h
postexplantation, and then in neuronal cells, with a peak at 24 h
after explantation when expression of viral replicative genes was
first detectable. Since ocular HSV-1 infection, corneal scarification,
and explantation of trigeminal ganglia all resulted in induction of
expression of cellular transcription factors in ganglia, these factors
may play a critical role in the permissiveness of cells for HSV-1
replication during acute infection, latency, and reactivation.

PMID: 1649322 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

17: J Virol. 1989 Nov;63(11):4976-8.  Related Articles, Links  


Latent infections in spinal ganglia with thymidine kinase-deficient
herpes simplex virus.

Leist TP, Sandri-Goldin RM, Stevens JG.

Department of Microbiology and Immunology, University of California,
Los Angeles School of Medicine 90024-1747.

A herpes simplex virus type 1 variant [C239(TK-)] harboring a deletion
in the thymidine kinase (TK) gene was assessed for capacity to
establish latent infections. Outbred Swiss Webster mice were
inoculated on both hind footpads, and numbers of neurons expressing
latency-associated transcript and amounts of viral DNA in latently
infected lumbosacral spinal ganglia were scored. C239(TK-) established
levels of latent infection that were only slightly lower than those
found for either a TK rescued variant of this agent or the parent
wild-type KOS. However, in contrast to the TK+ viruses, C239(TK-)
could not be reactivated when spinal ganglia were cultured in vitro.
The results presented show that expression of the viral TK gene plays
no major role in establishment of the latent state but that it
functions during reactivation of latent virus from explanted ganglia
maintained in vitro.

PMID: 2552180 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

18: J Virol. 1985 Aug;55(2):410-6.  Related Articles, Links  


Establishment of latency in mice by herpes simplex virus 1
recombinants that carry insertions affecting regulation of the
thymidine kinase gene.

Sears AE, Meignier B, Roizman B.

Herpes simplex virus 1 recombinants carrying alpha-, beta-, and late
gamma (gamma 2)-regulated thymidine kinase (TK) genes were tested for
the ability to establish latency in BALB/c mice inoculated by the eye
route. The significant findings were as follows. Representatives of
alpha- and gamma 2-regulated TK recombinants all established and
maintained latent infections, but the efficiency was somewhat lower
than that of wild-type virus. Of the three alpha TK recombinants
tested, one (R316) spontaneously deleted portions of the inserted
sequences which conferred alpha regulation to the TK gene. The viruses
carrying these deletions expressed considerably lower TK activity than
did wild-type virus, i.e., 2 to 40% of the levels expressed by the
wild-type virus carrying the beta TK gene. However, the ability of
these viruses to establish latency was not related to the efficiency
of expression of the TK gene. These results indicate the following:
(i) conversion of the TK gene into an alpha or gamma 2 gene did not
preclude the establishment of latent infections; (ii) there was no
correlation between the levels of TK activity expressed in cell
culture and the ability to establish latency; and (iii) rearrangement
of the genome by insertions or deletions which interrupt gene domains
did not automatically result in an inability to establish latent
infections.

PMID: 2991566 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

19: Virus Res. 1989 Oct;14(2):95-106.  Related Articles, Links  

Detection of HSV-1 proteins prior to the appearance of infectious
virus in mouse trigeminal ganglia during reactivation of latent
infection.

Wroblewska Z, Savage K, Spivack JG, Fraser NW.

Wistar Institute, Philadelphia, PA 19104.

Following corneal inoculation of mice HSV-1 produces an acute
infection and establishes a latent infection in trigeminal ganglia.
The latent virus can be reactivated in vitro by explantation of
ganglionic tissue. Viral protein expression was studied in trigeminal
ganglia during acute infection of mice and explant reactivation of
latent infection. HSV-1 proteins were detectable by
immunoprecipitation and immunostaining, in mouse ganglia only from 3-5
days post infection. Although during explant reactivation it has been
demonstrated that at 24 h post-explant the trigeminal ganglia are all
infectious virus negative (Spivack, O'Boyle II and Fraser (1987) J.
Virol. 61, 3288-3291), we have found that three HSV-1 proteins, of 175
kDa, 110 kDa and 90 kDa, are present in latently infected trigeminal
ganglia as early as 6-21 h post explantation. Initially, only neuronal
cells were positive by immunostaining with anti HSV-1 polyclonal serum
for HSV-1 antigens, but at later times HSV-1 antigens were seen in non
neuronal cells as well. These proteins may play a role in the initial
stages of the reactivation process.

PMID: 2558462 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

20: Virology. 1995 Jan 10;206(1):633-40.  Related Articles, Links  

In situ DNA PCR and RNA hybridization detection of herpes simplex
virus sequences in trigeminal ganglia of latently infected mice.

Mehta A, Maggioncalda J, Bagasra O, Thikkavarapu S, Saikumari P,
Valyi-Nagy T, Fraser NW, Block TM.

Jefferson Cancer Institute, Thomas Jefferson University, Philadelphia,
Pennsylvania 19107.

The presence of herpes simplex virus (HSV-1) DNA in the trigeminal
ganglia of latently infected mice was detected by an in situ DNA
polymerase chain reaction (PCR), which includes a DNA:DNA
hybridization step (indirect in situ PCR). These results were compared
to the number of neurons possessing the HSV-1 latency associated
transcript (LAT), as detected by in situ RNA hybridization with LAT
probes. Sensitivity assays were shown to detect a single copy cellular
gene in 48% of neuronal cell bodies. The results suggest that in situ
PCR is an effective method to locate and detect HSV-1 within latently
infected neurons. Moreover, the number of neurons found to be
harboring HSV-1, by the method of in situ PCR, which does not depend
upon virus gene expression, is within threefold of the number detected
by in situ hybridization for LAT. Therefore, this report describes the
first detection of HSV-1 DNA in latently infected murine trigeminal
ganglia by the method of indirect in situ PCR, and compares the
findings to the number of neurons expressing LAT, as assessed by
conventional in situ hybridization.

PMID: 7831818 [PubMed - indexed for MEDLINE]

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