Reactivation Of Latent Virus Research Articles

Herpes Zoster DNA Vaccines with IL-7 and IL-33 Molecular Adjuvants Elicit Protective T Cell Immunity.

Herpes zoster (HZ), or shingles, is caused by the reactivation of latent varicella-zoster virus (VZV) from the sensory ganglia when VZV-specific T-cell immunity is decreased because of aging or immunosuppression. In the present study, we developed HZ DNA vaccine candidates encoding VZV proteins and cytokine adjuvants, such as IL-7 and IL-33. We immunized C57BL/6 mice with DNA plasmids encoding VZV glycoprotein E (gE), immediate early (IE) 63, or IE62 proteins and found that robust VZV protein-specific T-cell responses were elicited by HZ DNA vaccination. Co-administration of DNA plasmids encoding IL-7 or IL-33 in HZ DNA vaccination significantly enhanced the magnitude of VZV protein-specific T-cell responses. Protective immunity elicited by HZ DNA vaccination was proven by challenge experiments with a surrogate virus, vaccinia virus expressing gE (VV-gE). A single dose of HZ DNA vaccine strongly boosted gE-specific T-cell responses in mice with a history of previous infection by VV-gE. Thus, HZ DNA vaccines with IL-7 and IL-33 adjuvants strongly elicit protective immunity.

Mollaret Meningitis with High Level of Cytokines in CSF Successfully Treated by Indomethacin

A rare case of Mollaret meningitis characterized by four recurrent episodes of aseptic meningitis during the 3-year periods were reported. The patient showed high fever and severe headache accompanied by high level of cerebrospinal fluid (CSF) cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alfa (TNF-a). The symptoms and high CSF cytokines were dramatically resolved immediately after inducing indomethacin treatment. Reactivation of the latent virus is considered to be the cause of this rare disease and indomethacin is estimated to inhibit periodic abnormal generation of eicosanoid in the brain resulting in reducing fever and subsequent inflammation.

UK experience of herpes zoster vaccination can inform varicella zoster virus policies

UK experience of herpes zoster vaccination can inform varicella zoster virus policies

Recurring infection with ecologically distinct HPV types can explain high prevalence and diversity

The high prevalence of human papillomavirus (HPV), the most common sexually transmitted infection, arises from the coexistence of over 200 genetically distinct types. Accurately predicting the impact of vaccines that target multiple types requires understanding the factors that determine HPV diversity. The diversity of many pathogens is driven by type-specific or "homologous" immunity, which promotes the spread of variants to which hosts have little immunity. To test for homologous immunity and to identify mechanisms determining HPV transmission, we fitted nonlinear mechanistic models to longitudinal data on genital infections in unvaccinated men. Our results provide no evidence for homologous immunity, instead showing that infection with one HPV type strongly increases the risk of infection with that type for years afterward. For HPV16, the type responsible for most HPV-related cancers, an initial infection increases the 1-year probability of reinfection by 20-fold, and the probability of reinfection remains 14-fold higher 2 years later. This increased risk occurs in both sexually active and celibate men, suggesting that it arises from autoinoculation, episodic reactivation of latent virus, or both. Overall, our results suggest that high HPV prevalence and diversity can be explained by a combination of a lack of homologous immunity, frequent reinfections, weak competition between types, and variation in type fitness between host subpopulations. Because of the high risk of reinfection, vaccinating boys who have not yet been exposed may be crucial to reduce prevalence, but our results suggest that there may also be large benefits to vaccinating previously infected individuals.

Dermatological Complications After Solid Organ Transplantation.

Organ transplant recipients (OTRs) are a population at high risk for cutaneous adverse events. Their early recognition and appropriate treatment is an important component of the clinical management of OTRs and should be optimally dealt with by dermatologists working in the context of a transplant dermatology clinic. Skin examination should be a standard procedure before performing organ transplantation to assess conditions which may be difficult to manage after the transplant procedure has been performed or which may represent a contraindication to transplantation, e.g., malignant melanoma. It also offers an opportunity to educate patients on skin care after organ transplantation. Skin infections can occur at any time after organ transplantation and include viral, bacterial, and fungal opportunistic infections. The risk of reactivation of latent viruses, such as varicella-zoster virus (VZV) and cytomegalovirus (CMV), is high. Bacterial infections are frequent and may be caused by unusual agents such Actinomyces, Mycobacteria, Legionella, or Nocardia. A large spectrum of fungal infections may occur, ranging from superficial (e.g., dermatophytes) to deeper and more severe ones (Alternaria, Aspergillus, Cryptococcus, Histoplasma). Drug-related idiosyncratic reactions usually occur early after the introduction of the causative drug, e.g., hypersensitivity reaction to azathioprine. On the long-term run, cutaneous effects due to cumulative drug toxicity, e.g., sebaceous hyperplasia from cyclosporine, may appear. Rare immunologically driven inflammatory reactions may occur in OTRs such as GVH or autoimmune disease. Tumors are particularly frequent. Kaposi's sarcoma, associated with persistent human herpes virus 8 (HHV8) infection, and cutaneous anaplastic large-cell lymphoma (ALCL) occur early after transplantation. Other cancers, such as nonmelanoma skin cancer (NMSCs), associated with persistent human papillomavirus (HPV) infections, malignant melanoma, Merkel cell carcinoma, or adnexal tumors, manifest later with an incidence which is much higher than observed in the general population. The incidence increases further after a first NMSC occurs.

Lack of TNF-α signaling through p55 makes the mice more susceptible to acute infection but does not alter state of latency and reactivation of HSV-1

TNF-α has been shown to play an important role in pathogenesis and latency of HSV-1 infections. TNF-α signals through TNFR1 (p55) and TNFR2 (p75), and signaling through p55 generally results in gene activation leading to induction of inflammatory responses. Here, we studied the role of TNF-α signaling in latent virus reactivation in p55-knock out (KO) mouse model of ocular HSV-1 infection. We found that KO mice are more susceptible to HSV-1 infection compared to wild type C57Bl/6 mice. While the absence of TNFRI signaling enhanced the ganglion latent DNA content by two folds, there was no difference in the maintenance and reactivation of latent HSV-1. Strikingly, interfering with inflammatory responses through PGE2 synthesis by treating latently infected wild type mice with indomethacin (COX inhibitor) prior to UV-exposure prevented HSV-1 reactivation. These results suggest that reactivation of latent HSV-1 might result from the cumulative effects of a cascade of inflammatory cytokines including TNF-α.

The HIV-1 Tat Protein: Mechanism of Action and Target for HIV-1 Cure Strategies.

The general mechanism involved in Tat activation of RNA Polymerase II (RNAP II) elongation of the integrated HIV-1 was elucidated over 20 years ago. This mechanism involves Tat binding to the TAR RNA element that forms at the 5' end of viral transcripts and recruiting a general RNAP II elongation factor termed as PTEFb. This elongation factor consists of CDK9 and Cyclin T1, and when recruited by Tat to TAR RNA, CDK9 was proposed to phosphorylate the carboxyl terminal domain of RNAP II and thereby activate elongation. Research in the past two decades has shown that the mechanism of Tat action is considerably more complicated than this simple model. In metabolically active cells, CDK9 and Cyclin T1 are now known to be largely sequestered in a RNA-protein complex termed the 7SK RNP. CDK9 and Cyclin T1 are released from the 7SK RNP by mechanisms not yet fully elucidated and along with Tat, bind to TAR RNA and orchestrate the assembly of a Super Elongation Complex (SEC) containing several additional proteins. CDK9 in the SEC then phosphorylates multiple substrates in the RNAP II complex to activate elongation. Importantly for therapeutic strategies, CDK9 and Cyclin T1 functions are down-regulated in resting CD4+ T cells that harbor latent HIV-1, and their up-regulation is required for reactivation of latent virus. Current strategies for a functional cure of HIV-1 infection therefore are likely to require development of latency reversal agents that up-regulate CDK9 and Cyclin T1 function in resting CD4+ T cells.

Pain in the elderly and its association with latent Epstein-Barr virus reactivation

Background Stress promotes immune dysregulation, including reactivation of latent viral infections and inflammation. Immune dysregulation can have severe health consequences, including delayed wound healing, impaired responses to vaccination, development and progression of cancer, and onset of mood disorders. Little is known about how pain is associated with reactivation of herpesviruses. Objective To evaluate the effects of pain on reactivation of latent Epstein-Barr virus (EBV), c-reactive protein (CRP), and interleukin-6 (IL-6) after controlling for age, gender, body mass index (BMI), race and income. Methods 51 bereaved and 64 controls were examined for pain (SF-36_Pain_Subscale) and immune dysregulation (EBV antibody titers, CRP, and IL-6). Linear regression models, adjusted for age, gender, BMI, race, and income were used to examine the association between pain and immune dysregulation. Results Results showed that greater pain was associated with higher reactivation of EBV ( β = −0.30; p β = −0.22; p β = −0.14; p = 0.16). Moreover, being older was associated with reactivation of EBV ( β = 0.32; p β = 0.27; p β = 0.34; p Conclusion Our results add to growing evidence of how pain can promote immune dysregulation. To our knowledge, this study is the first to demonstrate an association between pain and reactivation of a latent herpesvirus, which provides important implications for health outcomes.

Zoster Vaccine Effectiveness Against Incident Herpes Zoster and Post-Herpetic Neuralgia In Elderly In The UK

Herpes zoster (HZ) is a painful skin rash that occurs most frequently in older adults and is caused by reactivation of latent varicella zoster virus (VZV). Its most common complication is post-herpetic neuralgia (PHN). The UK introduced zoster vaccination in the national immunization program in 2013. The vaccine was routinely offered to 70 year-olds and, as part of the catch-up, to 79 year-olds. This study assessed the vaccine effectiveness (VE) against HZ and PHN in elderly within the total population. This retrospective cohort study included subjects from birth cohorts 1943-1946 (routine) and 1934-1937 (catch-up) in the UK Clinical Practice Research Datalink (CPRD). Vaccinated subjects were compared to unvaccinated subjects using piecewise Cox regression model. HZ outcomes in community setting were analyzed, including HZ, PHN and other HZ complications (i.e. neurological but not PHN, ocular, disseminated and other). For the routine birth cohorts (79274 subjects), we found a VE for HZ of 76.4% (95% CI: 70.6%-81.1%) and for PHN of 68.3% (95% CI: 7.4%-89.1%) for the first 2 years of vaccination. For the subsequent 2+ years, the VE estimates of HZ was 56.1% (95% CI: 29.2%-72.7%). For the catch-up cohorts (48193 subjects), the VE estimates were comparable. We found insufficient evidence to determine the VE for other HZ complications. Within the total population, the HZ vaccine provided protection against HZ and PHN, but its protection declined over time. Immunosuppressed conditions need to be taken into account.

Assessment of the Potential Herpes Zoster and Post Herpetic Neuralgia Case Avoidance with Vaccination in the United States

BackgroundHerpes zoster (HZ), commonly referred to as shingles, is a reactivation of latent varicella zoster virus in patients previously infected. Clinical characteristics of HZ include painful rash with potential complications, including post herpetic neuralgia (PHN). Care for HZ and PHN incurs significant costs and vaccination is beneficial. The aim of this study was to compare the impact on HZ and PHN case avoidance of two HZ vaccines, an available live-attenuated zoster vaccine (zoster vaccine live [ZVL]) vs. a candidate non-live adjuvanted HZ subunit vaccine (HZ/su), in the US population.MethodsA Markov model called ZONA (ZOster ecoNomic Analyses) was developed following two age cohorts (≥60 years to represent the current ACIP recommendation and ≥65 years to represent the Medicare population) over their lifetimes from the year of vaccination. Demographic data were obtained from the US Census, whereas HZ incidence and the proportion of HZ individuals developing PHN were derived from published US-specific sources. Age-specific vaccine efficacy and waning rates were based on published clinical trial data. Vaccine coverage for both vaccines was assumed to be 30.6% and 34.2% in the two age cohorts, respectively, based on CDC data; compliance of the second dose of the HZ/su vaccine was 69%, based on data from clinical trials and Hepatitis B seconddose completion. Sensitivity analyses demonstrated robustness of the base analysis findings.ResultsIn the US, for cohorts of 66.83 million (M) persons aged 60+ and 47.76M aged 65+ it was estimated that the HZ/su vaccine would reduce the number of HZ cases by 2.12M and 1.55M in the two age cohorts, respectively, compared with 0.65M and 0.45M using the ZVL. Furthermore, the HZ/su vaccine would reduce the number of PHN cases by 0.23M and 0.18M in the two age cohorts, respectively, compared with 0.10M and 0.09 using the ZVL. The number needed to vaccinate to prevent one HZ case were 10 and 11, in the respective cohorts, using the HZ/su vaccine compared with 31 and 37, in the respective cohorts, using the ZVL.ConclusionDue to higher and sustained vaccine efficacy, the candidate HZ/su vaccine demonstrated superior public health impact in the US compared with the currently available ZVL.Disclosures B. J. Patterson, GSK: Employee and Shareholder, GSK stock options or restricted shares and Salary; Pennsylvania Pharmacists Association: Scientific Advisor, stipend; P. O. Buck, GSK: Employee and Shareholder, GSK stock options or restricted shares and Salary; J. Carrico, RTI Health Solutions: Employee, Salary GSK: Research Contractor, Research support; K. A. Hicks, RTI: Employee, Salary GSK: Research Contractor, Research support; D. Curran, GSK: Employee and Shareholder, GSK stock options or restricted shares and Salary; D. Van Oorschot, GSK: Employee, Salary; J. E. Pawlowski, GSK: Employee and Shareholder, GSK stock options or restricted shares and Salary; B. Y. Lee, GSK: Consultant, Consulting fee; B. P. Yawn, GSK: Consultant and Scientific Advisor, Consulting fee

BK virus replication in renal transplant recipients: Analysis of potential risk factors may contribute in reactivation

BackgroundConsidering the increasing problem of BK virus infection during post renal transplant surveillance, it is necessary to distinguish the main risk factors leading to reactivation of latent BK virus. Up to now, some probable risk factors have been investigated in some studies, but the results have been confusing and contradictory. ObjectivesThe goal of the present study was to determine the frequency and potential risk factors that may play a role in BK polyomavirus reactivation and nephropathy. Study designIn this cross-sectional study, 110 patients, who underwent consecutive transplantation between 2010 and 2013, were enrolled without preliminary screening. Urine and blood samples were taken, and quantitative Real-time PCR assay was used to detect and measure the viral load. Demographic and clinical characteristics of the patients who had BK viremia and/or viruria were documented. ResultsAmong 110 cases of renal transplant recipients, BK viruria and viremia were found in 54 (49%) and 22 people (20%) respectively. The pre-transplant durations of dialysis among patients with BK viruia were found longer in comparison to BK negative patients. Treatment with Tacrolimus (p=0.03) was found to be a risk factor for development of BK viruria. In patients with viruria and viremia the median creatinine levels were 1.45mg/dl and 1.35mg/dl respectively, which were higher than those in the patients with negative results for BK viruria (p=0.002) and viremia (p=0.02). Also, treatment with Cyclosporine could significantly increase the incidence of BK virus shedding in both urine and blood among patients who received it (p=0.01). Significant relation between reactivation of BK virus and other factors such as age, sex, acute rejection and diabetes was not found. ConclusionBased on our findings, the main potential risk factors for shedding of BK virus into urine in renal transplant recipients were prolonged pre-transplant dialysis and Tacrolimus regimen. Cyclosporine regimens could be considered as risk factor for both BK viruria and viremia. A significant correlation between BK virus replication and elevated creatinine level was seen among our patients.

Is There any Seasonal Influence of Herpes Zoster?

Herpes zoster is a neurocutaneous disease caused by varicella zoster virus (VZV). It results from the reactivation of latent virus in dorsal root or cranial nerve cells following primary infection or vaccination as a consequence of waning of immunity. There may be a possible association between the occurrence of varicella infection and various environmental factors. So this study was designed to know the pattern of clinical presentation, seasonal variations and epidemiological factors of Herpes Zoster patients. A total of 172 Herpes Zoster out of 27979 patients of different skin diseases attending at Dhamrai Upazilla Hospital in Bangladesh were studied between March 2010 to June 2013. The frequency of occurrence of Herpes Zoster was 0.61%. Among the patients, 57.56% were male and 42.44% were female between the ages of 5 months to 90 years, with mean age 39 years. Nearly half of the patients (48.26%) were in between 30-59 years age. The patients were continued to report throughout the year with a surge in rainy season. Majority of the patients (65.70%) had thoracic dermatome followed by cervical and lumbar distribution, each of them 11%. A large-scale and prospective community based study is recommended to enrich the findings as well as a complete clinical and epidemiological picture of Herpes zoster in Bangladesh.Faridpur Med. Coll. J. Jan 2017;12(1): 14-17

Latent Cytomegalovirus (CMV) Infection Does Not Detrimentally Alter T Cell Responses in the Healthy Old, But Increased Latent CMV Carriage Is Related to Expanded CMV-Specific T Cells.

Human cytomegalovirus (HCMV) primary infection and periodic reactivation of latent virus is generally well controlled by T-cell responses in healthy people. In older donors, overt HCMV disease is not generally seen despite the association of HCMV infection with increased risk of mortality. However, increases in HCMV DNA in urine of older people suggest that, although the immune response retains functionality, immunomodulation of the immune response due to lifelong viral carriage may alter its efficacy. Viral transcription is limited during latency to a handful of viral genes and there is both an IFNγ and cellular IL-10 CD4+ T-cell response to HCMV latency-associated proteins. Production of cIL-10 by HCMV-specific CD4+ T-cells is a candidate for aging-related immunomodulation. To address whether long-term carriage of HCMV changes the balance of cIL-10 and IFNγ-secreting T-cell populations, we recruited a large donor cohort aged 23–78 years and correlated T-cell responses to 11 HCMV proteins with age, HCMV IgG levels, latent HCMV load in CD14+ monocytes, and T-cell numbers in the blood. IFNγ responses by CD4+ and CD8+ T-cells to all HCMV proteins were detected, with no age-related increase in this cohort. IL-10-secreting CD4+ T cell responses were predominant to latency-associated proteins but did not increase with age. Quantification of HCMV genomes in CD14+ monocytes, a known site of latent HCMV carriage, did not reveal any increase in viral genome copies in older donors. Importantly, there was a significant positive correlation between the latent viral genome copy number and the breadth and magnitude of the IFNγ T-cell response to HCMV proteins. This study suggests in healthy aged donors that HCMV-specific changes in the T cell compartment were not affected by age and were effective, as viremia was a very rare event. Evidence from studies of unwell aged has shown HCMV to be an important comorbidity factor, surveillance of latent HCMV load and low-level viremia in blood and body fluids, alongside typical immunological measures and assessment of the antiviral capacity of the HCMV-specific immune cell function would be informative in determining if antiviral treatment of HCMV replication in the old maybe beneficial.

Vaccine profile of herpes zoster (HZ/su) subunit vaccine

ABSTRACTIntroduction: Herpes zoster (HZ) causes an often severe and painful rash in older people and may be complicated by prolonged pain (postherpetic neuralgia; PHN) and by dissemination in immune-compromised patients. HZ results from reactivation of latent varicella-zoster virus (VZV) infection, often associated with age-related or other causes of decreased T cell immunity. A live attenuated vaccine boosts this immunity and provides partial protection against HZ, but this decreases with age and declines over 8 years.Areas covered: A new HZ subunit (HZ/su) vaccine combines a key surface VZV glycoprotein (E) with a T cell-boosting adjuvant system (AS01B) and is administered by two intramuscular injections two months apart.Expert commentary: HZ/su showed excellent efficacy of ~90% in immunocompetent adults ≥50 and ≥70 years of age, respectively, in the ZOE-50 and ZOE-70 phase III controlled trials. Efficacy was unaffected by advancing age and persisted for >3 years. Approximately 9.5% of subjects had severe, but transient (1–2 days) injection site pain, swelling or redness. Compliance with both vaccine doses was high (95%). The vaccine will have a major impact on HZ management. Phase I-II trials showed safety and immunogenicity in severely immunocompromised patients. Phase III trial results are expected soon.

Latent virus reactivation in astronauts on the international space station

Reactivation of latent herpes viruses was measured in 23 astronauts (18 male and 5 female) before, during, and after long-duration (up to 180 days) spaceflight onboard the international space station . Twenty age-matched and sex-matched healthy ground-based subjects were included as a control group. Blood, urine, and saliva samples were collected before, during, and after spaceflight. Saliva was analyzed for Epstein–Barr virus, varicella-zoster virus, and herpes simplex virus type 1. Urine was analyzed for cytomegalovirus. One astronaut did not shed any targeted virus in samples collected during the three mission phases. Shedding of Epstein–Barr virus, varicella-zoster virus, and cytomegalovirus was detected in 8 of the 23 astronauts. These viruses reactivated independently of each other. Reactivation of Epstein–Barr virus, varicella-zoster virus, and cytomegalovirus increased in frequency, duration, and amplitude (viral copy numbers) when compared to short duration (10 to 16 days) space shuttle missions. No evidence of reactivation of herpes simplex virus type 1, herpes simplex virus type 2, or human herpes virus 6 was found. The mean diurnal trajectory of salivary cortisol changed significantly during flight as compared to before flight (P = 0.010). There was no statistically significant difference in levels of plasma cortisol or dehydoepiandosterone concentrations among time points before, during, and after flight for these international space station crew members, although observed cortisol levels were lower at the mid and late-flight time points. The data confirm that astronauts undertaking long-duration spaceflight experience both increased latent viral reactivation and changes in diurnal trajectory of salivary cortisol concentrations.

Nanoparticle exposure reactivates latent herpesvirus and restores a signature of acute infection

BackgroundInhalation of environmental (nano) particles (NP) as well as persistent herpesvirus-infection are potentially associated with chronic lung disease and as both are omnipresent in human society a coincidence of these two factors is highly likely. We hypothesized that NP-exposure of persistently herpesvirus-infected cells as a second hit might disrupt immune control of viral latency, provoke reactivation of latent virus and eventually lead to an inflammatory response and tissue damage.ResultsTo test this hypothesis, we applied different NP to cells or mice latently infected with murine gammaherpesvirus 68 (MHV-68) which provides a small animal model for the study of gammaherpesvirus-pathogenesis in vitro and in vivo. In vitro, NP-exposure induced expression of the typically lytic viral gene ORF50 and production of lytic virus. In vivo, lytic viral proteins in the lung increased after intratracheal instillation with NP and elevated expression of the viral gene ORF50 could be detected in cells from bronchoalveolar lavage. Gene expression and metabolome analysis of whole lung tissue revealed patterns with striking similarities to acute infection. Likewise, NP-exposure of human cells latently infected with Epstein-Barr-Virus also induced virus production.ConclusionsOur results indicate that NP-exposure of persistently herpesvirus-infected cells – murine or human – restores molecular signatures found in acute virus infection, boosts production of lytic viral proteins, and induces an inflammatory response in the lung – a combination which might finally result in tissue damage and pathological alterations.

Benzotriazoles Reactivate Latent HIV-1 through Inactivation of STAT5 SUMOylation

SUMMARYThe presence of latent HIV-1 in infected individuals represents a major barrier preventingviral eradication. For that reason, reactivation of latent viruses in the presence of antiretroviral regimens has been proposed as a therapeutic strategy to achieve remission. We screened for small molecules and identified several benzotriazole derivatives with the ability to reactivate latent HIV-1. In the presence of IL-2, benzotriazoles reactivated and reduced the latent reservoir in primary cells, and, remarkably, viral reactivation was achieved without inducing cell proliferation, T cell activation, or cytokine release. Mechanistic studies showed that benzotriazoles block SUMOylation of phosphorylated STAT5, increasing STAT5’s activity and occupancy of the HIV-1 LTR. Our results identify benzotriazoles as latency reversing agents and STAT5 signaling and SUMOylation as targets for HIV-1 eradication strategies. These compounds represent a different direction in the search for “shock and kill” therapies.

Epigenetic regulation of cellular and cytomegalovirus genes during myeloid cell development.

Myeloid cells are important cell types that carry human cytomegalovirus. Latent viral DNA is present in CD34+ progenitor cells and their derived monocytes. However, differentiation of latently infected monocytes to mature macrophages or dendritic cells causes reactivation of latent viruses. During hematopoietic development, pluripotent genes are repressed, and lineage specific genes are activated in a step-wise manner. This process is governed by cell-type specific chromatin states. Enhancers in the hematopoietic system are highly dynamic and established by pioneer (first tier) transcription factors (TFs), which set the stage for second and third tier TF binding. In this review, we examine the epigenetic mechanisms that regulate myeloid cell development, cell identity, and activation with a special focus on factors that regulate viral gene expression and the status of viral infection in myeloid cells.

Palatal ulceration: A local anesthetic complication

The hard palate is one of the common sites of local complications following administration of local anesthetics. The hard, unyielding palatal tissues coupled with either forceful or excessive administration of solution, induction of trauma, use of contaminated solutions, or reactivation of latent viruses may present or aggravate local complications in the palatal area. Ulceration and necrosis is unusual and a rare complication of local anesthesia. Presented is such an uncommon case in a 16-year-old girl.

Ramsay hunt syndrome: A diagnostic challenge for general dental practitioners

Ramsay hunt syndrome is not just a syndrome but it's rather an infectious disease caused by reactivation of latent varicella-zoster virus in geniculate ganglion. This was first explained by J. Ramsay Hunt as a triad of complications like otalgia, mucosal and cutaneous rashes with or without trigeminal facial palsy. The facial palsy can occur with characteristic vesicles along the path of nerve. We present a case of Ramsay Hunt syndrome in a 48-year-old male. The unilateral pattern of facial involvement and presence of vesicles assisted us for early diagnosis, distinguishing the syndrome with diseases mimicking other severe neurological illnesses and prompt treatment.