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At least 37 records · Page 2Linked to original sources
PubMed2003

The gammaherpesvirus 68 latency-associated nuclear antigen homolog is critical for the establishment of splenic latency.

Open reading frame 73 (ORF 73) is conserved among the gamma-2-herpesviruses (rhadinoviruses) and, in Kaposi's sarcoma-associated herpesvirus (KSHV) and herpesvirus saimiri (HVS), has been shown to encode a latency-associated nuclear antigen (LANA). The KSHV and HVS LANAs have also been shown to be required for maintenance of the viral genome as an episome during latency. LANA binds both the viral latency-associated origin of replication and the host cell chromosome, thereby ensuring efficient partitioning of viral genomes to daughter cells during mitosis of a latently infected cell. In gammaherpesvirus 68 (gammaHV68), the role of the LANA homolog in viral infection has not been analyzed. Here we report the construction of a gammaHV68 mutant containing a translation termination codon in the LANA ORF (73.STOP). The 73.STOP mutant virus replicated normally in vitro, in both proliferating and quiescent murine fibroblasts. In addition, there was no difference between wild-type (WT) and 73.STOP virus in the kinetics of induction of lethality in mice lacking B and T cells (Rag 1(-/-)) infected with 1000 PFU of virus. However, compared to WT virus, the 73.STOP mutant exhibited delayed kinetics of replication in the lungs of immunocompetent C57BL/6 mice. In addition, the 73.STOP mutant exhibited a severe defect in the establishment of latency in the spleen of C57BL/6 mice. Increasing the inoculum of 73.STOP virus partially overcame the acute replication defected observed in the lungs at day 4 postinfection but did not ameliorate the severe defect in the establishment of splenic latency. Thus, consistent with its proposed role in replication of the latent viral episome, LANA appears to be a critical determinant in the establishment of gammaHV68 latency in the spleen post-intranasal infection.

Animals↗
PubMed2003

Varicella-zoster virus ORF47 protein kinase, which is required for replication in human T cells, and ORF66 protein kinase, which is expressed during latency, are dispensable for establishment of latency.

Varicella-zoster virus (VZV) results in a lifelong latent infection in human sensory and cranial nerve ganglia after primary infection. VZV open reading frame 47 (ORF47) and ORF66 encode protein kinases that phosphorylate several viral proteins, including VZV glycoprotein gE and ORF32, ORF62, and ORF63 proteins. Here we show that the ORF47 protein kinase also phosphorylates gI. While ORF47 is essential for virus replication in human T cells and skin, we found the gene to be dispensable for establishment of latent infection in dorsal root ganglia of rodents. ORF66 protein is expressed during latency. Rodents infected with VZV unable to express ORF66 developed latent infection at a rate similar to that for the parental virus. ORF63 transcripts, a hallmark of VZV latency, were also detected in similar numbers of animals infected with the ORF47 and ORF66 mutants and with the parental virus. VZV mutants unable to express four of the six genes that do not have herpes simplex virus (HSV) homologs (ORFs 1, 13, 32, 57) were also unimpaired for establishment of latency. While a truncated HSV VP16 mutant was previously reported to be unable to establish latency in a mouse model, we found that VZV with a deletion of ORF10, the homolog of HSV VP16, was dispensable for establishment of latency. Thus, seven genes, including one expressed during latency, are dispensable for establishing latent VZV infection.

Animals↗
PubMed2003

Distal motor latency and residual latency as sensitive markers of anti-MAG polyneuropathy.

There is debate whether the terminal latency index (TLI) is a sensitive marker for polyneuropathy with anti-myelin-associated-glycoprotein antibodies (anti-MAGP). We examined 6 patients with an anti-MAGP and 6 patients with a chronic inflammatory demyelinating polyneuropathy (CIDP). The electroneurographic features studied were: distal compound motor action potential (CMAP), distal motor latency (DML), motor conduction velocity (MCV) elbow to wrist (distal MCV), MCV axilla to elbow (proximal MCV), MCV distal/proximal, terminal latency index (TLI), residual latency (RL), F-wave, and modified F ratio. We found significant differences between anti-MAGP and CIDP for DML and for RL. No significant differences were found for TLI and the other measures. The TLI values were not significant probably because our patients had a longer duration of disease,which supports the hypothesis of a distal to proximal progression of conduction slowing over time. We propose that a residual latency >4.0 and a distal motor latency >7.0 are strongly suggestive for an anti- MAGP.

Action Potentials↗
PubMed2004

Prolonged P300 latency in thyroid failure: a paradox. P300 latency recovers later in mild hypothyroidism than in severe hypothyroidism.

This study was performed to analyze quantitatively the cognitive functions of patients with mild and severe hypothyroidism by measuring P300 event-related evoked potentials before and after euthyroidism was established. Patients diagnosed as having Hashimato's thyroiditis with thyroid stimulating hormone (TSH) levels between 5 and 10 mU/L (mild thyroid failure; n = 24) and those with severe hypothyroidism (n = 13) were enrolled randomly to the study protocol. P300-event related potentials were recorded during thyroid insufficiency, and in the first and sixth month of euthyroidism. P300 latencies were prolonged in both the mild and severe hypothyroid patients compared to controls (p = 0.042, p < 0.001, respectively). The overt hypothyroid patients showed significant decrease in their P300 latencies after the first month of euthyroidism (p = 0.001). These P300 latency values did not differ in the subsequent 6-month period. The mild hypothyroid group, however, displayed no improvement of P300 latency in the first month but normalized at the sixth month of euthyroidism. In conclusion, both the overt and the mild hypothyroid patients revealed prolonged P300 latencies. Unexpectedly, P300 latencies in the patients with mild thyroid failure required more time to recover compared to the overt hypothyroid patients. This finding indicates different clinical outcomes of various thyroid insufficiency states on the brain.

Adult↗
PubMed1997

Measurement of P300 and sleep characteristics in patients with hypersomnia: do P300 latencies, P300 amplitudes, and multiple sleep latency and maintenance of wakefulness tests measure different factors?

To explore further the relationship between ease of falling asleep, ability to maintain wakefulness, attention and information processing in sleep apnea and other sleep disorders, we conducted a thorough analysis of the similarities, differences and correlations between auditory and visual P300 amplitudes and latencies, and tests of sleepiness. The 283 consecutive patients presenting with hypersomnia were administered nocturnal polysomnography. Next day they underwent auditory and visual P300 recordings, Multiple Sleep Latency Test (MSLT) and Maintenance of Wakefulness Test (MWT). Correlation coefficients were calculated between auditory and visual P300 amplitudes and latencies, respiratory disturbance index (RDI), sleep efficiency, % stage 1, and the tests for sleepiness. Factor analysis was performed with data from P300 testing, MSLT and MWT. Auditory P300 amplitude was correlated with sleep efficiency. Auditory P300 latency was correlated with % stage 1, RDI, MSLT and MWT. Visual P300 latency was correlated with % stage 1, sleep efficiency and MWT. MSLT but not MWT was negatively correlated with sleep efficiency. Factor analysis suggests three factors: attention, information processing, and sleepiness. We conclude that P300 latencies and tests of sleepiness (MSLT and MWT) measure different abilities in patients with diagnosable disorders of daytime sleepiness.

Adult↗
PubMed1996

Single-trial latency variability does not contribute to fast habituation of the long-latency averaged auditory evoked potential in the albino rat.

Fast habituation (FH) is defined as a general reduction in long-latency, vertex-recorded, averaged auditory evoked potential (AEP) amplitude that occurs in response to the second of a pair of acoustic stimuli. Our laboratory has been studying FH in a variety of human populations with different paradigms and has interpreted it to be a measure of neural attentional mechanism(s) and/or resource allocation related to the processing of cognitive information. We have also reported an analogous phenomenon in the rat. In the present investigation, we examined the relationship between FH (viz., averaged AEP component amplitude decrement) and the single-trial latency variability of the AEP peaks comprising that component. Specifically, AEPs were obtained to 60 paired-tone stimuli from unanesthetized and restrained albino rats previously implanted with chronic skull electrodes. Using a template-matching algorithm similar to that used by Michalewski et al. (Electroenceph. clin. Neurophysiol., 1986,65:59-71), the latency variability for each animal was computed for the N1 and P2 peaks of the single-trial AEPs that were used to compose the averaged wave form. Findings indicated that (a) there was no difference in single-trial latency variability for these peaks either within or across tones, and (b) there was no relationship between single-trial latency variability for either the N1 or the P2 peaks and the overall peak-to-peak amplitude (N1-P2) of the averaged wave from in response to the second tone. Thus, FH of the N1-P2(i.e. Peak 2) amplitude in the rat is not due to an increase in latency variability across tones.

Acoustic Stimulation↗
PubMed1996

Downstream regulatory elements increase acute and latent herpes simplex virus type 2 latency-associated transcript expression but do not influence recurrence phenotype or establishment of latency.

The role of putative promoter or activator sequences downstream of the herpes simplex virus type 2 latency-associated transcript (LAT) promoter and upstream of the LAT intron was investigated in vivo by constructing and evaluating mutant viruses with deletions in this region. The deletion of LAT promoter sequences upstream of the primary LAT transcript reduced levels of LAT expression during productive infections, compared with the LAT expression level of wild-type virus, and abolished LAT expression during latency. The deletion of the putative downstream regulatory elements reduced but did not eliminate LAT expression during productive and latent infections. The deletion of both regions almost completely eliminated acute LAT transcription, although additional acute LAT-region transcription directed by sequences upstream of either region was detected by reverse transcriptase PCR. The deletion of the downstream elements did not influence the ability of the virus to reactivate from latently infected guinea pigs relative to the ability of the wild-type virus to reactivate; thus, decreased LAT expression did not affect the frequency of recurrence. The deletion of both regions did not affect the ability of the virus to establish latency. We conclude that downstream regulatory elements are necessary for maximal acute LAT expression but do not constitute an independent promoter during latency and do not play an obvious role in the establishment of our reactivation from latency.

Animals↗
PubMed1997

The herpes simplex virus type 1 latency-associated transcript gene regulates the establishment of latency.

Herpes simplex virus type 1 establishes latent infections in sensory neurons. During latency only one locus, the latency-associated transcript (LAT), is abundantly transcribed. Several lines of evidence suggest that this locus is required for the efficient reactivation from latency in experimental models. However, it is not yet clear whether this is a direct effect on the reactivation process per se or, as we have suggested, an indirect effect resulting from a decreased efficiency of establishment of latent infections. In this report wild-type and genetically engineered viral mutants were analyzed in a mouse model using a recently developed approach to precisely quantify latently infected neurons. It was found that strain KOS/M established latent infections, as defined by the presence of the viral genome, in about 30% of the neurons. Thirty-three percent of the mice with this latent viral burden reactivated in vivo following hyperthermic stress. In contrast, mutants in which either the basal LAT promoter or the 5' end of the LAT gene was deleted established latency in only 10% of trigeminal neurons (P < 0.00001), and these mice were impaired for reactivation. Repair of the locus resulted in wild-type levels of establishment and reactivation, mapping this function to the LAT region. Finer mapping demonstrated that a 2.3-kb fragment that contains the major LAT transcripts was sufficient to promote efficient establishment and subsequent reactivation when expressed in the context of a foreign gene. Hyperthermic stress applied during the first 3 days postinfection resulted in greatly increased numbers of neurons harboring the latent viral genome. This approach was found to increase the level of establishment of LAT-null mutants to that normally achieved by wild-type KOS/M. These establishment-repaired mice reactivated with wild-type efficiency. Thus, the LAT gene serves to increase the number of neurons in which latency is established, and no direct role for the LAT locus in reactivation could be demonstrated.

Animals↗
PubMed2004

Wide variations in herpes simplex virus type 1 inoculum dose and latency-associated transcript expression phenotype do not alter the establishment of latency in the rabbit eye model.

The latency-associated transcript (LAT) is required for efficient reactivation of herpes simplex virus type 1 from latent infection in the rabbit eye model, but LAT's mechanism of action is unknown. In addition to reactivation, the LAT region seems to correspond to multiple functions, with some LAT deletion mutants exhibiting increased virulence, increased neuronal death, and restricted establishment of latency. While a LAT promoter deletion mutant (17DeltaPst) seems to be primarily restricted in reactivation in the rabbit, subtle effects on virulence or the establishment of latency cannot be precluded at the normal high levels of virus inoculum used in the rabbit model. Since such additional LAT phenotypes may be more evident with lower doses of virus, we evaluated the influence of initial viral inoculum and LAT expression on the progression of acute infection and the establishment of latency. We have assayed both virus recovery rates and viral genome loads in rabbit corneas and trigeminal ganglia. Our results show that (i) in the corneas and trigeminal ganglia, the maximum amount of virus present during acute infection is independent of the LAT genotype and inoculum dose, although greater viral yields are obtained earlier with higher inoculum doses, and (ii) the range in numbers of latent genomes detected in the ganglia is independent of the inoculum dose and the LAT genotype and therefore no difference in establishment of latency is observed.

Animals↗
PubMed2005

Varicella-zoster virus ORF4 latency-associated protein is important for establishment of latency.

Varicella-zoster virus (VZV) encodes at least six genes that are expressed during latency. One of the genes, ORF4, encodes an immediate-early protein that is present in the virion tegument. ORF4 RNA and protein have been detected in latently infected human ganglia. We have constructed a VZV mutant deleted for ORF4 and have shown that the gene is essential for replication in vitro. The ORF4 mutant virus could be propagated when grown in cells infected with baculovirus expressing the ORF4 protein under the human cytomegalovirus immediate-early promoter. In contrast, the VZV ORF4 deletion mutant could not be complemented in cells expressing herpes simplex virus type 1 (HSV-1) ICP27, the homolog of ORF4. Cells infected with baculovirus expressing ORF4 did not complement an HSV-1 ICP27 deletion mutant. VZV-infected cotton rats have been used as a model for latency; viral DNA and latency-associated transcripts are expressed in dorsal root ganglia 1 month or more after experimental infection. Cotton rats inoculated with VZV lacking ORF4 showed reduced frequency of latency compared to animals infected with the parental or ORF4-rescued virus. Thus, in addition to VZV ORF63, which was previously shown to be critical for efficient establishment of latency, ORF4 is also important for latent infection.

Animals↗
PubMed2005

Induction of Kaposi's sarcoma-associated herpesvirus latency-associated nuclear antigen by the lytic transactivator RTA: a novel mechanism for establishment of latency.

Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiological agent contributing to development of Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman desease. Following primary infection, latency is typically established. However, the mechanism by which KSHV establishes latency is not understood. We have reported that the latency-associated nuclear antigen (LANA) can repress RTA (for replication and transcription activator) expression by down-regulating its promoter. In this study, we show that RTA is associated with the virion particle. We also show that RTA can activate the LANA promoter and induce LANA expression in transient reporter assays. Additionally, the transcription of RTA correlates with LANA expression in the early stages of de novo infection of KSHV, and induction of LANA transcription is responsive to induction of RTA with an inducible system. This induction in LANA transcription was dependent on recombination signal sequence binding protein Jkappa (RBP-Jkappa), as a RBP-Jkappa-deficient cell line was significantly delayed and inefficient in LANA transcription with expression of RTA. These studies suggest that RTA contributes to establishment of KSHV latency by activating LANA expression in the early stages of infection by utilizing the major effector of the Notch signaling pathway RBP-Jkappa. This describes a feedback mechanism by which LANA and RTA can regulate each other and is likely to be a key event in the establishment of KSHV latency.

Antigens, Viral↗
PubMed2004

Morphological and latency abnormalities of the mid-latency auditory evoked responses in schizophrenia: a preliminary report.

INTRODUCTION: Evoked potential (EP) amplitude and latency abnormalities have been extensively examined in schizophrenia. Morphological abnormalities of the mid-latency auditory evoked responses (MLAERs; P50, N100, P200), on the other hand, received very little attention. METHODS: Based on a priori defined set of morphological criteria, the morphology and latency of the MLAERs were blindly compared between stable outpatients with schizophrenia (N=27) and age- and gender-matched healthy control subjects (N=22). The morphology of the MLAERs was considered abnormal if one or more of the components fell outside the expected latency range, if one or more of the components were missing, or if a later occurring component was smaller in amplitude than an earlier occurring one. RESULTS: Of the 27 schizophrenia subjects, 20 had waveforms that were deemed atypical, while only 8 from the control group were classified as atypical (chi(2)=5.52, p<0.02). The latencies of the P50 and N100 components, identified based on morphology, were significantly prolonged in schizophrenia patients. CONCLUSIONS: These preliminary data suggest that morphological abnormalities of the MLAERs in schizophrenia patients are significant and should be taken into consideration when examining the MLAERs of this patient population.

Adult↗
PubMed2000

[Changes of latency and amplitude of short latency somatosensory evoked potentials during slow induction of anesthesia with sevoflurane].

In the present study, changes of latency and amplitude of short latency somatosensory evoked potentials (SSEPs) were evaluated continuously during slow induction of anesthesia from sevoflurane awake to deep levels of anesthesia in eight scheduled surgical patients. Not consistent with other previous investigations, the latency of N20 was significantly shortened with sevoflurane after 25 minutes from the beginning of inhalation compared with the awake control levels. No increase of latency was observed. The amplitudes of N20 were decreased with sevoflurane anesthesia in relation to duration of anesthesia. These results suggest that sevoflurane alone might have no marked pharmacological properties to change the latency of SSEPs even in the deep level of anesthesia.

Anesthesia, Inhalation↗
PubMed1994

Regulation of the herpes simplex virus latency-associated transcripts during establishment of latency in sensory neurons in vitro.

The temporal appearance of the major latency-associated transcript (LAT) of herpes simplex virus, type-1 (HSV-1) was examined in sensory neuronal cultures during the establishment of either a latent or a lytic infection. Under conditions that result in the establishment of a latent infection, a significant delay in LAT accumulation was observed. The delay in the appearance of LAT was reflected in both a reduced number of LAT-positive neurons detected by in situ hybridizations and by low levels of the major 2-kb LAT detected by Northern blot analysis at early times compared to later in the latent infection. The percentage of LAT-positive neurons shown by in situ hybridizations and the relative abundance of the major LAT by Northern blot analysis increased markedly by 14 days after inoculation with virus. In addition to the major LAT, a spliced 1.5-kb LAT species was detected in Northern blot analysis after establishment of latency in the neuronal cultures, similar to observations in vivo. In contrast to the latent infection, under conditions that produced lytic infections in the neuronal cultures, LAT and HSV-1-specific antigens were detected in the majority of neurons 24 hr after inoculation with virus. These results indicate that LAT expression during the establishment of latency is regulated differently than during the lytic infection: LAT expression appears to be inhibited initially during the establishment of latency, whereas LAT is readily expressed during the lytic infection.

Animals↗
PubMed1994

The latency-associated transcript gene of herpes simplex virus type 1 (HSV-1) is required for efficient in vivo spontaneous reactivation of HSV-1 from latency.

During herpes simplex virus type 1 (HSV-1) neuronal latency, the only viral RNA detected is from the latency-associated transcript (LAT) gene. We have made a LAT deletion mutant of McKrae, an HSV-1 strain with a very high in vivo spontaneous reactivation rate. This mutant (dLAT2903) lacks the LAT promoter and the first 1.6 kb of the 5' end of LAT. dLAT2903 was compared with its parental virus and with a rescued virus containing a restored LAT gene (dLAT2903R). Replication of the LAT mutant in tissue culture, rabbit eyes, and rabbit trigeminal ganglia was similar to that of the rescued and parental viruses. On the basis of semiquantitative PCR analysis of the amount of HSV-1 DNA in trigeminal ganglia, the LAT mutant was unimpaired in its ability to establish latency. In contrast, spontaneous reactivation of dLAT2903 in the rabbit ocular model of HSV-1 latency and reactivation was decreased to approximately 33% of normal. This decrease was highly significant (P < 0.0001) and demonstrates that in an HSV-1 strain with a high spontaneous reactivation rate, deletion of LAT can dramatically decrease in vivo spontaneous reactivation. We also report here that deletion of LAT appeared to eliminate rather than just reduce in vivo induced reactivation.

Animals↗
PubMed1995

Two herpes simplex virus type 1 latency-active promoters differ in their contributions to latency-associated transcript expression during lytic and latent infections.

Herpes simplex virus type 1 (HSV-1) establishes latency in human sensory ganglia, during which time the viral genome is transcriptionally silent with the exception of the latency-associated transcripts (LATs). The most abundant LAT is a 2-kb RNA whose biosynthesis is poorly characterized. The 2-kb LAT may be a primary transcript, or its synthesis may involve splicing and/or other forms of processing. Two potential RNA polymerase II promoters (LAP1 and LAP2) upstream of the 2-kb LAT 5' end have been identified. To investigate the role played by LAP1 and LAP2 in the synthesis of the 2-kb LAT under lytic and latent conditions, we analyzed HSV-1 mutants which contain deletions of one or both of these promoters. During lytic infection in cell culture, the cis elements critical for the normal accumulation of the 2-kb LAT were mapped to LAP2, while LAP1 sequences were largely dispensable. The 5' ends of the major 2-kb LATs produced by the wild-type and LAP deletion viruses were examined by primer extension analysis and were all found to be identical (+/- 2 bp). The accumulation of the 2-kb LAT during latent infections of murine trigeminal ganglia was examined by Northern (RNA) blot and by reverse transcription-PCR. In contrast to the results found in lytic infections, the critical cis elements needed for 2-kb LAT accumulation during latency were mapped to LAP1. Deletion of LAP1 resulted in a 500-fold reduction in 2-kb LAT accumulation, whereas deletion of LAP2 resulted in only a 2- to 3-fold reduction. Deletion of both LAP1 and LAP2 resulted in undetectable levels of the 2-kb LAT. Our results indicate that both LAP1 and LAP2 are critical for 2-kb LAT expression but under different conditions. LAP1 is essential for LAT expression during latency, while LAP2 is primarily responsible for LAT expression in lytic infections in cell culture. LAP1 and LAP2 may prove to be functionally independent promoter elements that control 2-kb LAT expression during different stages of HSV-1 infections.

Animals↗
PubMed2004

Kaposi's sarcoma-associated herpesvirus-encoded latency-associated nuclear antigen inhibits lytic replication by targeting Rta: a potential mechanism for virus-mediated control of latency.

Like other herpesviruses, Kaposi's sarcoma-associated herpesvirus (KSHV, also designated human herpesvirus 8) can establish a latent infection in the infected host. During latency a small number of genes are expressed. One of those genes encodes latency-associated nuclear antigen (LANA), which is constitutively expressed in cells during latent as well as lytic infection. LANA has previously been shown to be important for the establishment of latent episome maintenance through tethering of the viral genome to the host chromosomes. Under specific conditions, KSHV can undergo lytic replication, with the production of viral progeny. The immediate-early Rta, encoded by open reading frame 50 of KSHV, has been shown to play a critical role in switching from viral latent replication to lytic replication. Overexpression of Rta from a heterologous promoter is sufficient for driving KSHV lytic replication and the production of viral progeny. In the present study, we show that LANA down-modulates Rta's promoter activity in transient reporter assays, thus repressing Rta-mediated transactivation. This results in a decrease in the production of KSHV progeny virions. We also found that LANA interacts physically with Rta both in vivo and in vitro. Taken together, our results demonstrate that LANA can inhibit viral lytic replication by inhibiting expression as well as antagonizing the function of Rta. This suggests that LANA may play a critical role in maintaining latency by controlling the switch between viral latency and lytic replication.

Antigens, Viral↗
PubMed2004

The herpes simplex virus type 1 latency-associated transcript (LAT) enhancer/rcr is hyperacetylated during latency independently of LAT transcription.

During herpes simplex virus type 1 (HSV-1) latency, only one region of the viral genome is actively transcribed: the region encoding the latency-associated transcript (LAT). A previous study demonstrated that during latency the LAT promoter is hyperacetylated at histone H3 (K9, K14) relative to lytic genes examined. In the present study, we examine the acetylation profile of regions downstream of the LAT promoter during a latent infection of murine dorsal root ganglia. These analyses revealed the following: (i) the region of the genome containing the 5' exon of the LAT primary transcript was at least as enriched in acetylated H3 as the LAT promoter, and (ii) the region of hyperacetylation does not extend to the ICP0 promoter. In order to assess the contribution of LAT transcription to the acetylation of the 5' exon region, the acetylation profile of KOS/29, a recombinant with a deletion of the LAT promoter, was examined. The region containing the 5' exon of KOS/29 was hyperacetylated relative to lytic gene regions in the absence of detectable LAT transcription. These results indicate that the region containing the 5' exon of LAT, known to contain enhancer activities and to be critical for induced reactivation (rcr), exists in a chromatin structure during latency that is distinct from other lytic gene regions. This result suggests a role for the 5' exon LAT enhancer region as a cis-acting regulator of transcription that maintains a transcriptionally permissive chromatin domain in the HSV-1 latent episome.

Acetylation↗