Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GANGLIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMed1996

The Effect of Parasitism by Fasciola hepatica and Muellerius capillaris on the Nerve Ganglia of Lymnaea truncatula

Morphometric and histopathological studies were performed in Lymnaea truncatula experimentally infected by Fasciola hepatica or Muellerius capillaris between Days 30 and 60 postinfection. In the pedal ganglia, snail parasitism had a significant influence on the decrease in length and the increase in width in the M. capillaris group. In the dorsal lobes of cerebral ganglia, snail parasitism had a significant influence on the decrease in lobe width in the F. hepatica group and the increase in width in the M. capillaris group. In the two groups of infected snails, snail parasitism had a significant influence on the decrease in the number of neurons in the pedal ganglia and the dorsal lobes of the cerebral ganglia. The other ganglia and lobes did not demonstrate any significant differences in the size or number of neurons. Infected snails of both groups had multifocal nerve lesions, i.e. (a) dyskariosis with occasionally eccentric nuclei and (b) cell lysis with only cell remnants present.

Journal Article↗
PubMed1983

Quantitative autoradiographic studies of 5-HT-accumulating neurones in the nodose ganglia of the cat after perikaryal or terminal uptake.

The distributions of ganglionar cell bodies, specifically labeled with 3H-5-HT, were studied in light microscope autoradiographs of the cat nodose ganglion. The size, number and localization of labeled cells were examined under different experimental conditions: after in vitro incubation of the ganglion with 3H-5-HT and after retrograde transport of 3H-5-HT injected into the nucleus of the solitary tract (NST) which receives primary visceral sensory projections from nodose ganglia cells of the vagal nerve. Following incubation of the nodose ganglia with a low concentration of 3H-5-HT (10(-6) M), some ganglionar cell bodies took up and retained the tracer. In both the right and left ganglia, they were significantly smaller in size than the unreactive neurones. The mean diameter of their perikaryon was 36.97 +/- 0.52 microns, compared with 45.76 +/- 0.87 microns in unreactive neurones. About 600 labeled cell bodies were counted in each ganglion, corresponding to 2-3% of the total nodose ganglion cell population. These reactive neurones were not localized in one particular area of the ganglia, but scattered throughout both of them. Following bilateral or unilateral microinjections of 3H-5-HT in the NST, retrogradely labeled cell bodies were observed, 24 h later, in the nodose ganglia. Their mean diameter was estimated to be 36.14 +/- 0.69 microns and they represented approximately 2% of the total ganglion cell population. As in in vitro experiments, the labeled cells were not grouped in any particular region of the ganglion. These experiments show that the distribution of both populations of labeled cells, observed under these conditions, are comparable. On an anatomical and quantitative basis one may reasonably suppose that the perikaryal or terminal uptakes concern the same neuronal population.

Animals↗
PubMed1992

Cardiac responses elicited by stimulation of loci within stellate ganglia of developing swine.

Stimulation with bipolar electrodes of specific loci in stellate ganglia elicited in anesthetized piglets, 1-4 weeks of age, alterations in cardiac function and aortic pressure. Responses were also elicited by chemical stimulation in specific loci of these ganglia. The probability of eliciting a cardiovascular response by stimulating loci in a stellate ganglion increased with increasing postnatal age. For instance, no responses were elicited when loci in the left stellate ganglia of 1-week-old piglets were stimulated. Significant heart rate responses were obtained only when loci in right stellate ganglia were stimulated. The number of ganglionic loci from which cardiovascular responses were obtained increased with increasing postnatal age. It is concluded that the capacity of stellate ganglion neurons to modulate the cardiovascular system matures during the first four weeks of life, heart rate being modulated primarily by neurons in the right stellate ganglion and inotropism by neurons in both stellate ganglia.

Aging↗
PubMed1989

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

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.

Animals↗
PubMed1999

Expression of BDNF and TrkB mRNAs in the crista neurosensory epithelium and vestibular ganglia following ototoxic damage.

Following ototoxic lesion with the aminoglycoside gentamicin, the vestibular neurosensory epithelia undergo degeneration and then limited spontaneous regeneration. The spatio-temporal expression of brain-derived neurotrophic factor (BDNF) and of its high affinity receptor (trkB) mRNA was investigated in the vestibular end organs and ganglia of chinchillas following gentamicin ototoxicity. In the vestibular ganglia of untreated chinchillas, the level of expression of BDNF mRNA is low. At 1 and 2 weeks after intraotic treatment with gentamicin, BDNF mRNA levels in the vestibular ganglia were elevated significantly compared to untreated chinchillas and chinchillas 4 weeks after treatment. At 4 weeks after gentamicin treatment, BDNF mRNA levels were at intact levels of expression. In the crista ampullaris, high levels of BDNF transcripts were found in the untreated chinchillas. At 1 and 2 weeks after treatment, when only supporting cells are present in the crista, BDNF mRNA was undetectable. Four weeks after aminoglycoside treatment BDNF mRNA was present in the epithelium but at lower levels than in the intact epithelium. In contrast to its ligand, high levels of trkB mRNA hybridization were present in the vestibular ganglia of untreated chinchillas and trkB mRNA levels did not change following gentamicin treatment. In the vestibular epithelia, trkB mRNA was not detected either in the intact epithelium or after gentamicin ototoxicity. These data suggest that BDNF may be involved in the maintenance of the vestibular ganglia and contribute to neurite outgrowth to new and repaired hair cells following ototoxic damage.

Animals↗
PubMed1998

Highly variable distribution of HSV-1-specific DNA in human geniculate, vestibular and spiral ganglia.

Viral reactivation in temporal ganglia is the suspected cause of Bell's palsy, vestibular neuritis and sudden hearing loss. Since the distribution of latent herpes simplex type 1 (HSV-1) in geniculate, vestibular and spiral ganglia of individual human temporal bones could have implications for the explanation of isolated as well as combined disorders of these three cranial nerves, we examined these ganglia in 18 human temporal bones of adults by nested polymerase chain reaction. In all of the temporal bones HSV-1 specific DNA was detected: 10/18 (56%) of the geniculate, 11/18 (61%) of the vestibular and 9/18 (50%) of the spiral ganglia samples were positive. All combinations of positive and negative ganglia were found in individual temporal bones at roughly equal frequencies. These data support a viral etiology of all three conditions, especially their occasional combinations.

Adult↗
PubMed2000

The indirect basal ganglia pathway in dopamine D(2) receptor-deficient mice.

Recent pathophysiological models of basal ganglia function in Parkinson's disease predict that specific neurochemical changes in the indirect pathway would follow the lack of stimulation of D(2) dopamine receptors. Post mortem studies of the basal ganglia in genetically modified mice lacking functional copies of the D(2) dopamine receptor gene allowed us to test these predictions. When compared with their congenic N(5) wild-type siblings, mice lacking D(2) receptors show an increased expression of enkephalin messenger RNA in the striatum, and an increased activity and expression of cytochrome oxidase I in the subthalamic nucleus, as expected. In addition, D(2) receptor-deficient mice display a reduced expression of glutamate decarboxylase-67 messenger RNA in the globus pallidus, as the basal ganglia model predicts. This reduction contrasts with the lack of change or increase in glutamate decarboxylase-67 messenger RNA expression found in animals depleted of dopamine after lesions of the mesostriatal dopaminergic system. Furthermore, D(2) receptor-deficient mice show a significant decrease in substance P messenger RNA expression in the striatonigral neurons which form the direct pathway. Finally, glutamate decarboxylase-67 messenger RNA expression in the basal ganglia output nuclei was not affected by mutations in the D(2) receptor gene, a fact that could probably be related to the absence of a parkinsonian locomotor phenotype in D(2) receptor-deficient mice. In summary, these findings provide compelling evidence demonstrating that the lack of endogenous stimulation of D(2) receptors is sufficient to produce subthalamic nucleus hyperactivity, as assessed by cytochrome oxidase I histochemistry and messenger RNA expression, and strongly suggest the existence of interactions between the basal ganglia direct and indirect pathways.

Animals↗
PubMed1978

Virology and histopathology of the trigeminal ganglia of Americans and Japanese.

Herpes simplex virus in the trigeminal ganglia of humans was studied in Philadelphia, Pennsylvania, United States of America, and in Kyoto, Japan. The prevalence of recurrent herpes labialis and of clinically latent herpes simplex virus within trigeminal ganglia was determined in inhabitants of the two cities. In addition, a comparison was made of the prevalence of mononuclear cell infiltration in the trigeminal ganglia of Americans and Japanese. Recurrent herpes labialis was found to be significantly less common in the Japanese city than in the American city. Herpes simplex virus was rescued less commonly from the trigeminal ganglia of cadavers in Japan than in America. The difference was significant. The frequency of mononuclear cell infiltration in the trigeminal ganglia of Americans and Japanese is not significantly different. These observations, as well as previously reported serological studies, suggest that despite the ubiquitous nature of herpes simplex virus in America and Japan, the Japanese have less clinically overt disease caused by this virus.

Adolescent↗
PubMed1997

beta-Gal enzyme activity driven by the HSV LAT promoter does not correspond to beta-gal RNA levels in mouse trigeminal ganglia.

beta-Galactosidase enzyme expression can be detected in only a small percentage of trigeminal ganglia (TG) neurons acutely and latently infected with herpes simplex virus (HSV), in which the lacZ reporter gene was placed down-stream of the latency associated transcript (LAT) promoter at the LAT locus. However, DNA quantification suggests that a larger percentage of cells is infected than is expressing beta-galactosidase enzyme. To investigate the mechanism involved in regulation of genes expressed from the LAT promoter in trigeminal ganglia, in situ hybridization and histochemical staining assays were employed to determine on a cell-by-cell basis beta-gal gene expression both at the RNA and protein level. Using a LAT promoter-driven beta-gal construct in HSV-1 strain HFEM, it was found that there were 89-fold more cells positive for beta-gal transcript than cells positive for beta-gal enzyme in acutely infected trigeminal ganglia and a 10-fold difference in latently infected trigeminal ganglia. Thus, there is a discordance between beta-gal mRNA and beta-gal enzyme levels in HFEM/LAT-lacZ infected cells during acute and latent infection, and the beta-gal reporter gene activity does not faithfully compare the LAT promoter activity between acute and latently infected tissue. In contrast, in situ hybridization and histochemical staining assays were performed in mice acutely infected with a virus in which 140 bp of the LAT promoter sequences flanking the TATA element were replaced by 1.8 kbp of the neurofilament promoter (HSV-1 HFEM/NF-lacZ). This construct showed a correlation between beta-gal mRNA and enzyme expression in trigeminal ganglia in acute and latent infections. These findings suggest that sequences at the 5' end of the beta-gal transcript influence translation of the beta-gal message.

Animals↗
PubMed1989

Thymidine kinase-negative herpes simplex virus mutants establish latency in mouse trigeminal ganglia but do not reactivate.

Herpes simplex virus infection of mammalian hosts involves lytic replication at a primary site, such as the cornea, translocation by axonal transport to sensory ganglia and replication, and latent infection at a secondary site, ganglionic neurons. The virus-encoded thymidine kinase, which is a target for antiviral drugs such as acyclovir, is not essential for lytic replication yet evidently is required at the secondary site for replication and some phase of latent infection. To determine the specific stage in viral pathogenesis at which this enzyme is required, we constructed virus deletion mutants that were acyclovir resistant and exhibited no detectable thymidine kinase activity. After corneal inoculation of mice, the mutants replicated to high titers in the eye but were severely impaired for acute replication in trigeminal ganglia and failed to reactivate from ganglia upon cocultivation with permissive cells. Nevertheless, latency-associated transcripts were expressed in neuronal nuclei of ganglia from mutant-infected mice and superinfection of the ganglia with a second virus rescued the latent mutant virus. Thus, contrary to a widely accepted hypothesis, the thymidine kinase-negative mutants established latent infections, implying that neither thymidine kinase activity nor ganglionic replication is necessary for establishment of latency. Rather, thymidine kinase appears to be necessary for reactivation from latency. These results suggest that acyclovir-resistant viruses could establish latent infections in clinical settings and have implications for the use of genetically engineered herpesviruses to deliver foreign genes to neurons.

Acyclovir↗
PubMedDate not supplied

Ganglia in children.

Sixty-one children with ganglia treated surgically at the Singapore General Hospital were reviewed. At the wrist the predominance of dorsal ganglia over volar ganglia, which is the pattern in adults, was found only in older children. In children less than 10 years old, volar ganglia predominated. A high recurrence rate (36%) following surgery was observed, putting in question the value of surgery. An expectant regimen is therefore advocated at first. A modified technique for excision of volar wrist ganglia without attendant risk to the radial vessels is discussed.

Adolescent↗
PubMed1991

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.

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.

Animals↗
PubMed1999

Latency-associated transcripts of equine herpesvirus type 4 in trigeminal ganglia of naturally infected horses.

Equine herpesvirus type 4 (EHV-4) is a major respiratory pathogen of horses. Unlike most other members of the Alphaherpesvirinae, EHV-4 was regarded as non-neurotropic. Here, neural and lymphoid tissues of 17 horses have been analysed post-mortem. EHV-4 DNA was detected in 11 cases (65%) by PCR, exclusively in the trigeminal ganglia. In order to define the transcriptional activity, RNA preparations of 10 EHV-4 DNA-positive ganglia were investigated by nested RT-PCR. EHV-4-specific transcripts derived from genes 63 [herpes simplex virus type 1 (HSV-1) ICPO gene homologue] and 64 (HSV-1 ICP4 gene homologue) were detected in six trigeminal ganglia. In one other case, only gene 64-specific transcripts were present. All of the transcripts proved to be antisense orientated when a strand-specific RT-PCR was applied. Type-specific primers for gene 33 (encoding glycoprotein B) served to detect transcripts of an acute EHV-4-infection, which were found in only one of the six ganglia positive for gene 63- and gene 64-specific transcripts. Overall, these studies clearly demonstrate that EHV-4 is latent in trigeminal ganglia.

Animals↗
PubMed1995

Bradykinin receptors in mouse and rat isolated superior cervical ganglia.

1. The ability of bradykinin and its analogues to depolarize rat and mouse superior cervical ganglia was studied by use of in vitro grease-gap recording techniques, and the ability of antagonists selective for bradykinin receptor subtypes to block their effects was examined. 2. Bradykinin (3 microM) depolarized ganglia from both species, although the magnitude of the maximal response was less in mouse (15 +/- 5%, n = 7) than rat tissue (33 +/- 6%, n = 7), relative to muscarine (1 microM). 3. Interleukin 1 beta (30 u ml-1 for 18 h at 37 degrees C) increased the depolarization caused by bradykinin (3 microM) in mouse ganglia from 15% to 54% (P < 0.001, n = 12). Responses to the B1 receptor agonist, [des-Arg10]-kallidin (3 microM) were similarly potentiated but this was only detected after inhibition of peptidase activity with 10 microM captopril (4% to 35%, n = 5). 4. In ganglia from both species the rank order of agonist potency was bradykinin = [Lys0]-bradykinin >> [des-Arg10]-kallidin. However, like responses to [des-Arg10]-kallidin in mouse tissue, both the potency of bradykinin and the maximal depolarization achieved (EC50 = 912 nM; 80%, n = 11) was enhanced following inhibition of angiotensin converting enzyme with 10 microM captopril (EC50 = 50 nM; 135%, n = 4). 5. Responses to bradykinin were selectively antagonized by the B2 receptor antagonist, Hoe 140 but not by the B1 antagonist, [Leu8]-bradykinin1-8. From Schild analysis the pA2 value for Hoe 140 in mouse tissue was 9.65, although the slope of the regression line was significantly greater than unity, indicating non-competitive kinetics (slope = 1.88 +/- 0.18, n = 9). The depolarization caused by [Lys0]-bradykinin was also antagonized by Hoe 140 (3 nM).6. Thus the predominant bradykinin receptor in mouse superior cervical ganglia is compatible with a B2 subtype. Furthermore the depolarizations caused by B1 and B2 agonists in this tissue can be increased following exposure to interleukin l beta, and by blocking peptide degradation with captopril.

Amino Acid Sequence↗
PubMed1980

Induction of 2',5'-oligoadenylate synthetase and interferon in mouse trigeminal ganglia infected with herpes simplex virus.

The activity of 2',5'-oligoadenylate synthetase, which is induced by interferon action, was detected in mouse trigeminal ganglia infected with herpes simplex virus (HSV) type 1. When HSV was inoculated on the left cheek of mice, the virus began to appear in the ipsilateral trigeminal ganglia on day 2, reached its maximum accumulation on day 4, declined thereafter, and was no longer detected in the tissue homogenate after 11 days. After this short acute productive phase, the virus entered into the latent phase of infection. 2',5'-Oligoadenylate synthetase appeard in the trigeminal ganglia shortly after the beginning of virus multiplication; the synthetase activity began to rise on day 3, reached a maxium level on day 4, and then declined. Interferon activity (type I) also appeared in the infected ganglia, but diminished more rapidly than the synthetase. The antibody against HSV in the sera began to appear at the time when the virus and synthetase were declining. From these results it may be hypothesized, although not concluded, that in the acute productive phase of HSV infection in mouse trigeminal ganglia, virus multiplication is suppressed by interferon action, including 2',5'-oligoadenylate synthetase induction.

2',5'-Oligoadenylate Synthetase↗
PubMed1988

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

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.

Animals↗
PubMed1990

A herpes simplex virus type 1 mutant containing a nontransinducing Vmw65 protein establishes latent infection in vivo in the absence of viral replication and reactivates efficiently from explanted trigeminal ganglia.

Vmw65, a herpes simplex virus type 1 (HSV-1) tegument protein, in association with cellular proteins, transactivates viral immediate early genes. In order to examine the role of Vmw65 during acute and latent infection in vivo, a mutant virus (in1814), containing a 12-base-pair insertion in the Vmw65 gene, which lacks the transactivating function of Vmw65 (C. I. Ace, T. A. McKee, J. M. Ryan, J. M. Cameron, and C. M. Preston, J. Virol. 63:2260-2269, 1989) was examined in mice. Following corneal inoculation, the parental virus (17+) and the revertant (1814R) replicated effectively in eyes and trigeminal ganglia with 30 to 60% mortality. At either equal PFU or equal particle numbers, in1814 did not replicate in trigeminal ganglia and none of the infected mice died. Although in1814 did not replicate following corneal inoculation, it established latent infection in trigeminal ganglia. HSV-1 in1814 reactivated at explant as efficiently and rapidly as did 17+ and 1814R. Even low amounts of inoculated in1814 (10(2) PFU) were sufficient to establish latent infection in some animals. Since infectious in1814 was not detected at any time in mouse trigeminal ganglia, in1814 provided a unique opportunity to determine how soon after primary infection latency begins. Latent in1814 infection was detected shortly after virus reached the sensory ganglia, between 24 to 48 h postinfection. Thus, though Vmw65 may be required for lytic infection in vivo, it is dispensable for the establishment of and reactivation from latent infection. These data support the hypotheses that the latent and lytic pathways of HSV-1 are distinct and that latency is established soon after infection without a requirement for viral replication. However, the levels of Vmw65 reaching neuronal nuclei may be a critical determinant of whether HSV-1 forms a lytic or latent infection.

Animals↗
PubMed2000

Analysis of individual human trigeminal ganglia for latent herpes simplex virus type 1 and varicella-zoster virus nucleic acids using real-time PCR.

Herpes simplex virus type 1 (HSV-1) and varicella-zoster virus (VZV) establish latent infections in the peripheral nervous system following primary infection. During latency both virus genomes exhibit limited transcription, with the HSV-1 LATs and at least four VZV transcripts consistently detected in latently infected human ganglia. In this study we used real-time PCR quantitation to determine the viral DNA copy number in individual trigeminal ganglia (TG) from 17 subjects. The number of HSV-1 genomes was not significantly different between the left and right TG from the same individual and varied per subject from 42.9 to 677.9 copies per 100 ng of DNA. The number of VZV genomes was also not significantly different between left and right TG from the same individual and varied per subject from 37.0 to 3,560.5 copies per 100 ng of DNA. HSV-1 LAT transcripts were consistently detected in ganglia containing latent HSV-1 and varied in relative expression by >500-fold. Of the three VZV transcripts analyzed, only transcripts mapping to gene 63 were consistently detected in latently infected ganglia and varied in relative expression by >2,000-fold. Thus, it appears that, similar to LAT transcription in HSV-1 latently infected ganglia, VZV gene 63 transcription is a hallmark of VZV latency.

Aged↗