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PlayAs if having a cold sore isn’t bad enough, some researchers believe that the virus that causes them can lead to prolonged cognitive damage.
That hitchhiking herpes virus that starts with cold sores confirms saga of ancient human migration around the world. The virus under study, herpes simplex virus type 1 (HSV-1), usually causes nothing more severe than cold sores around the mouth, says Curtis Brandt, a professor of medical microbiology and ophthalmology at the University of Wisconsin-Madison. From knowledge of how quickly a particular genome changes, they can construct a "family tree" that shows when particular variants had their last common ancestor.
Scientists have previously studied herpes simplex virus type 1 by looking at a single gene, or a small cluster of genes, but Brandt notes that this approach can be misleading. The technology of simultaneously comparing the entire genomes of related viruses could also be useful in exploring why certain strains of a virus are so much more lethal than others. For studies of influenza virus in particular, Brandt explains in the news release, "people are trying to come up with virulence markers that will enable us to predict what a particular strain of virus will do." The researchers broke the HSV-1 genome into 26 pieces, made family trees for each piece and then combined each of the trees into one network tree of the whole genome, Brandt says in the news release. But what really jumped out of the study, Brandt says in the news release, "was clear support for the out-of-Africa hypothesis.
Often a mother with an impending cold sore outbreak who's infectious but may not know it yet kisses a baby or toddler on the mouth and gives the child facial herpes for life, usually resulting in cold sores. Now the question is how did the first person acquire mouth herpes in the first place from what, where, and when?
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Homemade frugal solution to mirror and window cleaningThere are hundreds of products on the market that can and also claim they are great cleaning agents. Top of pageAbstractChronic pain is a major health concern with up to 50% of patients finding little if any relief following traditional pharmacotherapy.
Full figure and legend (49K)HSV is a large double-stranded DNA virus that in its natural life cycle is spread by contact, infecting and replicating in skin or mucous membrane.
Full figure and legend (95K)Opioid receptors are found presynaptically on the terminals of primary nociceptive afferents in the spinal cord, and postsynaptically on second-order neurons in the dorsal horn.
Full figure and legend (16K)Similar effects were subsequently demonstrated using a nonreplicating HSV vector deleted for both copies of the essential HSV IE gene ICP4. Contribution of thymidine kinase (TK) mutations to acyclovir (ACV) resistance were evaluated in herpes simplex type 1 recombinant viruses generated using a set of overlapping cosmids and plasmids.
Figure 1: Schematic representation of viral cosmids and plasmids used to generate HSV-1 recombinants into Vero cells. Figure 2: Replication kinetics of several HSV-1 mutants and the WT virus in a single-step growth experiment. Organisation of the herpes simplex virus type 1 genome, showing the origin of latency-associated transcripts.
So who was the first person to pass on the herpes virus--the type that causes cold sores, facial herpes outbreaks and herpes rashes found on the face, chest, arms, and back known as herpes simplex virus type 1?
Brandt is senior author of the study, now online as of October 16, 2013 published online in the journal PLOS ONE. We found that all of the African isolates cluster together, all the virus from the Far East, Korea, Japan, China clustered together, all the viruses in Europe and America, with one exception, clustered together," he says. Studies of human genomes have shown that our ancestors emerged from Africa roughly 150,000 to 200,000 years ago, and then spread eastward toward Asia, and westward toward Europe.
In a tiny percentage of cases, for example, HSV-1 can cause a deadly brain infection, Brandt notes. We believe that a difference in the gene sequence is determining the outcome, and we are interested in sorting this out," he says in the news release. Every HSV-1 sample from the United States except one matched the European strains, but one strain that was isolated in Texas looked Asian. But the herpes virus that entered on the lips could over a lifetime spread to the face, chest, arm, and back.
In the virus, as in human genomes, a small human population entered the Middle East from Africa. These studies were supported by grants from the National Institutes of Health: R01EY07336 and R01EY018597. Fink, Department of Neurology, University of Michigan and VA Ann Arbor Healthcare System, 1914 Taubman Center, 1500 E Medical Center Drive, Ann Arbor, Michigan 48109, USA.
This review describes the treatment of chronic pain using herpes simplex virus type 1 (HSV)-based vectors. In the setting of persistent injury, molecular, structural, and biochemical alterations in the properties of components of the pain pathway result in a syndrome of chronic pain.
Viral particles released in the skin are taken up by sensory nerve terminals and then carried by retrograde axonal transport to the neuronal perikaryon in the DRG, where the wild-type virus may either re-enter the lytic cycle, or establish a latent state from which the (wild-type) virus can subsequently reactivate and spread to other individuals. Activation of receptors naturally by endogenous ligands enkephalin or endomorphin (EM), or therapeutically by opiate drugs such as morphine, inhibits pain-related neurotransmission at the spinal level. Subcutaneous inoculation of an enkephalin-producing nonreplicating vector produces an analgesic effect in the delayed phase of the formalin model of inflammatory pain.10 The time course of the analgesic effect of this vector, maximal at 1 week and declining over time, is consistent with the known time course of expression driven by the human cytomegalovirus IE promoter (HCMV IEp) inserted to drive transgene expression from this vector. Alterations in both conserved and non-conserved regions of the TK gene were shown to confer high levels of resistance to ACV.Herpes simplex virus type 1 (HSV-1) and 2 (HSV-2) infections are associated with serious complications in immunocompromised hosts.
On the day of infection, confluent Vero cells in 12-well plates were infected with recombinant viruses at a MOI of 2.
A study of the full genetic code of a common human virus offers a dramatic confirmation of the "out-of-Africa" pattern of human migration, which had previously been documented by anthropologists and studies of the human genome. Furthermore, HSV-1 is much simpler than the human genome, which cuts the cost of sequencing, yet its genome is much larger than another virus that also has been used for this type of study. HSV can be effectively used to deliver pain-modulating transgenes to sensory neurons in vivo following intradermal inoculation. The efficacy of HSV-mediated gene transfer of enkephalin has been tested in several different models of pain in rodents (Figure 3). The observation that reinoculation of the vector at 4 weeks restored the analgesic effect is consistent with the interpretation that the animals do not develop tolerance to the vector-mediated transgene product released from synaptic terminals in vivo. Prolonged antiviral treatment is often required for the clinical management of these patients, which could lead to the emergence of drug-resistant viruses [222, 230]. Extracellular viruses were collected at different times post-infection (up to 120 h) and titrated onto Vero cells. Major LATs are introns of ~1.5 kb and ~2 kb that are spliced from mLAT as indicated in the figure.
Either the sample had come from someone who had traveled from the Far East, or it came from a native American whose ancestors had crossed the "land bridge" across the Bering Strait roughly 15,000 years ago. Genetics often comes down to a numbers game; larger numbers produce stronger evidence, so a larger genome produces much more detail. The vector genome persists in peripheral nerve bodies in an episomal state and serves as a platform for expression of natural pain-relieving molecules that access endogenous antinociceptive circuitry. Primary nociceptors are pseudounipolar neurons with cell bodies in the dorsal root ganglion (DRG) and axons that terminate peripherally in the skin or organs and project centrally to terminate in the dorsal horn of spinal cord in an anatomically defined (dermatomal or radicular) pattern. These gene functions can be classified as either essential for virus replication or accessory playing an important role in the natural history of virus infection in the host. The observations regarding reinoculation, which have been repeated in several different models of pain and with different transgene products, indicates the absence of any significant immune response to vector inoculation in the rodent.HSV-mediated enkephalin expression produces antinociceptive effects in neuropathic pain as well. Acyclovir (ACV), which has been the standard treatment for HSV infections, must be first phosphorylated by the viral thymidine kinase (TK) and then by cellular kinases before inhibiting the virus-encoded DNA polymerase (DNA pol) (reviewed in [442]). Drug resistance patterns of recombinant herpes simplex virus DNA polymerase mutants generated with a set of overlapping cosmids and plasmids. The vectors are mutated to prevent reactivation from latency or spread to the central nervous system. Second-order neurons project from the spinal cord principally to sensory nuclei in the thalamus. Two approaches have been used to construct recombinant HSV vectors for use in gene transfer. In clinic, HSV resistance to ACV is most commonly due to mutations (substitutions, deletions or additions) in the viral TK gene [233].
Dermatome selection for administration of HSV vectors provides targeted delivery of pain gene therapy to primary afferent neurons. Third-order neurons in the thalamus project to sensory cortex that subserves the discriminative aspects of pain perception, and to limbic cortex to subserve the hedonic aspects of the pain experience. Single base substitutions in the viral DNA pol gene have been more rarely reported in ACV-resistant clinical HSV isolates, with or without additional TK mutations [230, 286].

This novel approach alleviates pain without systemic side effects or the induction of tolerance and can be used in combination with standard pain treatments. Recombinant herpes viruses defective in tk can be propagated in culture and will replicate in skin, but are unable to replicate in the DRG and are thus forced into a pseudo-latent state. Because of the presence of multiple mutations within these two genes including several ones associated with viral polymorphism [230, 234, 249, 261, 446, 447], it has been difficult so far to analyze the contribution of each specific HSV mutation with regard to the ACV resistance phenotype. In addition to the ascending pathways, descending pathways that ultimately project from the brainstem back to the spinal dorsal horn act to modulate primary nociceptive neurotransmission at that first synapse in the pain pathway.Two categories of chronic pain are commonly distinguished. A second class of HSV vectors is rendered defective in essential virus genes and thus fails to replicate in all cell types. We recently reported the generation and characterization of HSV-1 DNA pol mutants [443] using a set of four overlapping cosmids and three plasmids based on the original work of Cunningham et al.
Attractive targets for deletion include the immediate-early (IE) class of genes that are required to launch the cascade of viral gene expression; recombinants deleted in these genes are blocked at the beginning of the replication cycle. Many factors including a drop in pH and release of inflammatory mediators such as histamine, bradykinin, endothelin, or interleukins (ILs) result in recruitment of inflammatory cells and continuous activation of nociceptors.
These gene products include infected cell polypeptides (ICPs) ICP4 and ICP27 without which the virus genome is highly repressed.3 Such recombinants can be propagated in cells that provide the missing gene product(s) in trans, but are incapable of replication in vivo4 (Figure 2). Herein, we report a modification of this cosmid-based recombination system to evaluate the impact of HSV-1 TK mutations as well as double TK-DNA pol mutations on the ACV resistance phenotype.Vero cells were maintained in minimum essential medium supplemented with 10 % fetal calf serum. Neuropathic pain is that pain which results from damage to neural structures, which arises in the absence of accompanying injury to non-neural tissues. The HSV-1 recombinant strain 17 and all mutant viruses derived from this strain were propagated in Vero cells. A common form of neuropathic pain occurs in diabetes, where nerve damage (diabetic neuropathy) is accompanied by spontaneously occurring pain. Replication of wild-type HSV requires the expression of essential immediate-early (IE) genes that are expressed on entry of the viral genome into the nucleus (a). EM-2 (Tyr-Pro-Phe-Phe-NH2) is an endogenous highly selective µ-receptor agonist,20 but the gene coding for EM-2 has not yet been identified.
The method used to generate HSV-1 recombinant viruses from overlapping cosmids (gift of Charles Cunningham, MRC Virology Unit, Glasgow, United Kingdom) as well as the plasmid used for site-directed mutagenesis of the viral DNA pol gene have been described elsewhere [443]. Highly reliable heterologous system for evaluating resistance of clinical herpes simplex virus isolates to nucleoside analogues. Recombinants for gene transfer are rendered replication incompetent by disruption of expression of one or more essential IE genes (indicated by black circle, b). We therefore constructed a tripartite synthetic gene cassette with the N-terminal signal sequence of human preproenkephalin followed by a pair of EM-2 coding elements including the addition a C-terminal glycine residue flanked by dibasic cleavage sites.
Neuropathic pain treatment regimens commonly employ anticonvulsant drugs that are used to reduce neuronal excitability and selective or nonselective serotonin reuptake inhibitors that, among other effects, modulate nociceptive neurotransmission in the dorsal horn. These replication-incompetent recombinants can be propagated to high titers in complementing cells engineered to express the required IE functions from the cellular genome (c).
The gene product is processed by the cellular machinery that processes preproenkephalin to enkephalin,21 with the C-terminal glycine in the cleaved product directing amidation of the cleaved peptide by the widely distributed enzyme peptidylglycine α-amidating monooxygenase. Isolation and characterization of deletion mutants of herpes simplex virus type 1 in the gene encoding immediate-early regulatory protein ICP4. Treatment of both nociceptive and neuropathic pain often ends in the use of opioid drugs that act at endogenous receptors at multiple sites in the neuraxis to modulate nociceptive neurotransmission.
Because the currently available drugs act through mechanisms that are not specific to pain-related neural pathways, off-target effects unrelated to the relief of pain often limit the maximum dose of analgesic medication that can be prescribed. In the special case of the potent opioid analgesic morphine, for example, activation of opioid receptors in regions of brain unrelated to pain perception results in somnolence, confusion, and ultimately impaired respiration, whereas activation of opioid receptors in the gut and the urinary bladder result in nausea, constipation, and urinary retention. In addition, continued treatment with opioids results in the development of tolerance leading to a requirement for escalating doses of medication to achieve the same result and treatment is further complicated by the possibility of drug abuse, unrelated to pain relief.The wide distribution of a limited range of neurotransmitters, receptors, and voltage-gated ion channels in the nervous system makes it difficult to selectively target pain-related pathways using drugs that are administered systemically. Specific mutations in the TK gene (located between nt 186 to nt 1007 of the viral gene) were introduced into plasmid pYS-1 using the Quickchange site-directed mutagenesis kit (Stratagene, La jolla, CA). Gene transfer methods have been used to achieve continuous expression of short-lived analgesic peptides at several sites in the ascending pain pathway.
In the selective SNL model of neuropathic pain, inoculation of the GAD-expressing vector results in a substantial reduction in mechanical allodynia and thermal hyperalgesia as shown in ref.
The first synapse between the primary nociceptor and the second-order projection neuron in the spinal cord is a particularly attractive target because of the ability to selectively block nociception at that level.
The correct nucleotide sequence of each mutated TK gene was verified by sequence analysis and compared to that of strain 17. In neuropathic pain, the analgesic effect of the GAD-expressing vector is greater in magnitude than the effect produced by either the enkephalin or EM-expressing vectors. Intrathecal administration results in a tenfold reduction in dose requirement and a reduction in off-target adverse events. This finding is consistent with the evidence that development of chronic pain after peripheral nerve injury is accompanied by the loss of GABAergic tone in the dorsal horn of spinal cord,27 and the clinical observation that opiate drugs are relatively ineffective in the treatment of neuropathic pain.
Briefly, digested cosmids (n = 4) and plasmids (n = 3) were transfected using Lipofectamine 2000 (Invitrogen, Burlington, ON, Canada) into Vero cells seeded in 12-well plates.
However, despite this directed approach, problems remain in effectiveness and tolerance.Over the past several years, a number of investigators have used herpes simplex virus (HSV)-based vectors to achieve a similar targeted delivery of inhibitory neurotransmitters at the spinal level to block nociceptive neurotransmission at the first synapse between the primary peripheral nociceptor and the second-order neuron in the spinal cord. HSV-based vectors have also been used to express anti-inflammatory cytokines to block central neuroimmune activation that appears to play an important role in the transition from acute pain perception to the chronic pain state, and more recently, have been employed to alter the expression or activation of ion channels involved in pain-sensing changes in the local environment. Therapeutic efficacy in experimental polyarthritis of viral-driven enkephalin overproduction in sensory neurons.
The TK and DNA pol sequences of each recombinant virus were again verified by DNA sequencing. These include the use of genes that encode antisense or microRNA sequences and genes that antagonize ion channel function whose activities are essential to the development of chronic pain. Inoculation of the vector 1 week before SNL delayed, but did not ultimately prevent, the development of neuropathic pain. Acyclovir susceptibility of each recombinant virus was determined by the use of a plaque reduction assay (PRA) [449].
Intrathecal injection of plasmid, adenovirus, and adeno-associated virus–based vectors has been tested in animal models of pain, but this review is limited to the published preclinical studies of HSV vectors in the treatment of chronic pain. A two-fold difference in IC50 values between the recombinant wild-type (WT) and mutant viruses was considered significant [443]. Evidence that the "active centre" of the herpes simplex virus thymidine kinase involves an interaction between three distinct regions of the polypeptide. The use of HSV vectors exploits the advantage of local vector application to the skin where virus entry into sensory nerve endings leads to vector transport to the nerve cell body. Met-enkephalin is preferentially transported into the peripheral processes of primary afferent fibres in both control and HSV1-driven proenkephalin A overexpressing rats. All experiments were done in duplicate using two independently-generated viruses for each mutation of interest. Replication kinetics of each recombinant mutant virus (tested in duplicate at a multiplicity of infection (MOI) of 2) were compared to that of the recombinant WT virus by titrating extracellular viruses collected at specific times post-infection (up to 120 h) onto Vero cells [443].Eight recombinant HSV-1 viruses (WT, TK-deleted, 4 TK mutants, 1 DNA pol mutant and 1 dual TK-DNA pol mutant), selected on the basis of their report in previous clinical or laboratory studies, were successfully generated in this study. Antinociceptive effect of a genomic herpes simplex virus-based vector expressing human proenkephalin in rat dorsal root ganglion. Nonreplicating recombinant HSV vectors injected into the skin (a) are carried by retrograde axonal transport to the dorsal root ganglion (DRG) (b) where the vector establishes a pseudo-latent state. All recombinant mutants were resistant to ACV with the single DNA pol mutant D907V being the less resistant (4-fold change in IC50 compared to WT) and the double TK (deleted C467 with truncated protein)-DNA pol (D907V) mutant being the most resistant (62-fold change in IC50). Transgene products produced in the DRG are released from afferent nerve terminals in the dorsal horn of spinal cord (c) to modulate nociceptive neurotransmission. Transgene-mediated enkephalin release enhances the effect of morphine and evades tolerance to produce a sustained antiallodynic effect.
2, the replication kinetics of the mutants were relatively similar to that of the WT virus up to 120 h post-infection. Attenuation of pain-related behavior in a rat model of trigeminal neuropathic pain by viral-driven enkephalin overproduction in trigeminal ganglion neurons. Our results obtained with recombinant viruses, which allows mutational studies in a homogeneous background, revealed that several mutations in conserved but also in non-conserved regions of the TK gene are associated with high levels of ACV resistance. It appears that the same mechanisms involved in shutoff of HSV gene expression during latency repress transgene expression in vivo. The mutation K62N, located in the ATP-binding site of the TK, conferred the highest level of resistance to ACV with the exception of the TK-deleted virus and the dual TK-DNA pol mutant.
In wild-type HSV, the latency-active promoter escapes promoter silencing to drive expression of the latency-associated transcript, a nonpolyadenylated RNA that can be detected years after primary infection.

The importance of the lysine at position 62 has been previously demonstrated in a site-directed mutagenesis study [450]. The latency-active promoter sequence has been identified as a transposable element49 that has been demonstrated to be capable of driving prolonged biologically active transgene expression in both the central50 and peripheral nervous system51,52 in rodents.The preclinical studies provide proof-of-principle for the potential utility of HSV-based vectors in the treatment of chronic pain.
Herpes simplex virus mediated nerve growth factor expression in bladder and afferent neurons: potential treatment for diabetic bladder dysfunction.
This mutation, also described in an ACV-resistant varicella-zoster virus isolate [451], has been associated with a TK-low producer phenotype.
The animal studies demonstrate that different genes can effectively be delivered to DRG by subcutaneous inoculation of HSV to provide analgesic effects in different models of pain. The mutation C336Y, implicated in the conformation of the TK protein, also resulted in a phenotype highly resistant to ACV. Although comparison of different models is difficult, it would appear that the most effective gene product may vary according to the type of pain being treated.
The latter mutation was first described in laboratory-derived ACV-resistant mutants [247, 253] but also in a TK-altered clinical HSV-2 isolate [287].
Experience garnered from studies of replication-compromised (but not incompetent) HSV vectors directly into brain in patients with glioblastoma have not demonstrated significant toxicity,53,54 suggesting that the intradermal inoculation of replication-incompetent vectors should be safe. Gene therapy of bladder pain with herpes simplex virus (HSV) vectors expressing preproenkephalin (PPE). Of interest, the mutation P131S, located in a non-conserved region of the TK gene, also conferred an ACV-resistant phenotype. A commonly expressed concern is whether the nonreplicating vector might recombine with endogenous viruses to produce a wild-type lytic virus carrying the transgene.
This mutation has been previously described in a laboratory-derived mutant passed in the presence of ACV [452]. For this reason, an HSV vector engineered for human use has been constructed to incorporate the transgene within the essential IE gene ICP4 locus; thus, a recombination event incorporating the transgene would render the recombinant replication incompetent.
Since this ACV-resistant mutant contained both the P131S TK mutation as well as a DNA pol mutation (A719V), our study was able to confirm the role of the former mutation in conferring resistance to ACV. Extensive preclinical biodistribution studies showed no evidence of vector spread from the site of inoculation, and, in parallel, toxicology studies showed no evidence of vector-induced toxicity. Treatment of inflamed pancreas with enkephalin encoding HSV-1 recombinant vector reduces inflammatory damage and behavioral sequelae. A single TK mutation (deletion of a C at position 467 leading to a truncated protein) induced high level of ACV resistance whereas the single DNA pol mutation D907V, within a non-conserved gene region, induced low level of resistance to ACV.
An IND for the first phase 1 human trial of HSV, to examine the well-characterized enkephalin-expressing nonreplicating HSV vector in patients with intractable pain caused by cancer, was approved by the Food and Drug Administration in February 2008. The recombinant virus containing the two previous mutations had the highest ACV IC50 value among all recombinant viruses confirming the synergistic effect of dual TK-DNA pol mutations. The simultaneous presence of these two mutations was reported in a HSV-2 isolate from a patient with AIDS in whom ACV and foscarnet therapy sequentially failed [230]. Acyclovir-resistant herpes simplex virus infections in patients with the acquired immunodeficiency syndrome. Enkephalin-encoding herpes simplex virus-1 decreases inflammation and hotplate sensitivity in a chronic pancreatitis model. Our study unequivocally shows that the deletion of a C at position 467 in a homopolymer run, which introduces a stop codon 25 amino acids downstream, was mainly responsible for the ACV resistance phenotype of this isolate.
Finally, as expected, the TK-deleted recombinant virus was highly resistant to ACV although not much more than single TK substitutions such as K62N and C336Y.Alterations in the TK are most frequently seen in clinic, probably because this protein is not essential for viral replication in most tissues and cultured cells [233, 234]. Murine models of inflammatory, neuropathic and cancer pain each generates a unique set of neurochemical changes in the spinal cord and sensory neurons. Indeed, the replication kinetics of all tested recombinant viruses including the TK-deleted virus were similar to that of the WT virus. In addition, mutation D907V, located in a non-conserved region of the DNA pol gene, did not affect viral replication in contrast to other previously-reported DNA pol mutations located within conserved gene regions [443]. In conclusion, we have developed a system that now allows rapid assessment of any mutations found in both viral genes associated with ACV resistance. Herpes vector-mediated expression of proenkephalin reduces pain-related behavior in a model of bone cancer pain. Such methodology could serve to develop virtual drug phenotypes for HSV with systematic evaluation of viral mutations found in clinical specimens. Phenotypic and genotypic characterization of acyclovir-resistant herpes simplex viruses from immunocompromised patients. Eur J Pain (epub ahead of print).Jones, TL, Sweitzer, SM, Wilson, SP and Yeomans, DC (2003).
Afferent fiber-selective shift in opiate potency following targeted opioid receptor knockdown.
Enhanced peripheral analgesia using virally mediated gene transfer of the mu-opioid receptor in mice. Peripherally delivered glutamic acid decarboxylase gene therapy for spinal cord injury pain.
Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cord.
An altered spectrum of herpes simplex virus mutations mediated by an antimutator DNA polymerase. Tumor necrosis factor-alpha induces mechanical allodynia after spinal nerve ligation by activation of p38 MAPK in primary sensory neurons. Polymorphisms of thymidine kinase gene in herpes simplex virus type 1: Analysis of clinical isolates from herpetic keratitis patients and laboratory strains. Tumor necrosis factor alpha contributes to below-level neuropathic pain after spinal cord injury.
Interleukin-4 (IL-4) inhibits secretion of IL-1 beta, tumor necrosis factor alpha, and IL-6 by human monocytes. Interleukin-4 and -13 inhibit tumor necrosis factor-alpha mRNA translational activation in lipopolysaccharide-induced mouse macrophages. Delivery to the central nervous system of a nonreplicative herpes simplex type 1 vector engineered with the interleukin 4 gene protects rhesus monkeys from hyperacute autoimmune encephalomyelitis. HSV-mediated expression of interleukin-4 in dorsal root ganglion neurons reduces neuropathic pain. HSV-mediated transfer of interleukin-10 reduces inflammatory pain through modulation of membrane tumor necrosis factor alpha in spinal cord microglia. The glial cell line-derived neurotrophic factor family receptor components are differentially regulated within sensory neurons after nerve injury.
HSV-mediated gene transfer of the glial cell derived neurotrophic factor (GDNF) provides an anti-allodynic effect in neuropathic pain. Decrease in inflammatory hyperalgesia by herpes vector-mediated knockdown of Nav1.7 sodium channels in primary afferents. Antihyperalgesic effect of a recombinant herpes virus encoding antisense for calcitonin gene-related peptide.
Role of genotypic analysis of the thymidine kinase gene of herpes simplex virus for determination of neurovirulence and resistance to acyclovir. PKC contributes to basal and sensitizing responses of Trpv1 to capsaicin in dorsal root ganglion neurons. Continuous delta opioid receptor activation reduces neuronal voltage gated sodium channel (NaV1.7) levels through activation of protein kinase C in painful diabetic neuropathy. Site-directed mutagenesis of a nucleotide-binding domain in HSV-1 thymidine kinase: effects on catalytic activity. Genetic characterization of thymidine kinase from acyclovir-resistant and susceptible herpes simplex virus type 1 isolated from bone marrow transplant recipients. Characterization of the DNA polymerase and thymidine kinase genes of herpes simplex virus isolates from AIDS patients in whom acyclovir and foscarnet therapy sequentially failed. Differential mutation patterns in thymidine kinase and DNA polymerase genes of herpes simplex virus type 1 clones passaged in the presence of acyclovir or penciclovir. Analysis of the thymidine kinase genes from acyclovir-resistant mutants of varicella-zoster virus isolated from patients with AIDS.

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