scholarly journals MANAGEMENT OF HSV-1 AND HSV-2 PRIMARY INFECTION IN ADULT PATIENT: A CASE REPORT

2021 ◽  
Vol 6 (1) ◽  
pp. 90
Author(s):  
Bima Ewando Kaban ◽  
Dahlia Riyanto ◽  
Adiastuti Parmadiati ◽  
Desiana Radithia ◽  
Bagus Soebadi
Keyword(s):  
Case Report ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
High Titer ◽  
Correct Diagnosis ◽  
Well Being ◽  
Immunoglobulin M ◽  
Viral Reactivation ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT Infection of Herpes Simplex Virus (HSV) type 1 and 2 causes medical problems throughout the world. HSV-1 infection often affects the oral regions and HSV-2 infection is the most prevalent cause of genital ulcerations.  It is possible for HSV-2 to cause oro-labial herpes and HSV-1 to cause genital herpes. Primary HSV infection usually affects children or adolescent, whereas adults usually experience infection more frequently due to viral reactivation. Objective:  To discuss the management of Primary HSV-1 and HSV-2 Infection which appears simultaneously in adults. Case report: a 33yearold female patient came to hospital with multiple painful ulcers in her tongue, buccal and labial mucosa, preceded by prodrome, followed with eruption and outbreak of vesicles on her skin. The first laboratory examination confirmed a high titer of reactive Immunoglobulin M (IgM) of anti-HSV-1 and Immunoglobulin M (IgM) anti-HSV-2. She was diagnosed to have Primary HSV-1 and HSV-2 Infection and treated with oral Acyclovir and Chlorine dioxide mouthwash with good healing. The clinical presentation, differential diagnosis and management of primary herpetic stomatitis are discussed. Conclusion: Correct diagnosis and treatment can restore well-being, avoid secondary problems for patients, and prevent the use of inappropriate drugs.Keywords : Herpes Simplex Virus, HSV-1, HSV-2, Management, Primary Herpes Infection

scholarly journals Herpes Simplex Virus Type 2 (HSV-2) Establishes Latent Infection in a Different Population of Ganglionic Neurons than HSV-1: Role of Latency-Associated Transcripts

2006 ◽  
Vol 81 (4) ◽  
pp. 1872-1878 ◽  
Author(s):  
Todd P. Margolis ◽  
Yumi Imai ◽  
Li Yang ◽  
Vicky Vallas ◽  
Philip R. Krause
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Dorsal Root Ganglia ◽  
Herpes Simplex Virus Type ◽  
Dorsal Root ◽  
Acute Infection ◽  
Viral Reactivation ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACTHerpes simplex virus type 1 (HSV-1) and HSV-2 cause very similar acute infections but differ in their abilities to reactivate from trigeminal and dorsal root ganglia. To investigate differences in patterns of viral infection, we colabeled murine sensory ganglia for evidence of HSV infection and for the sensory neuron marker A5 or KH10. During acute infection, 7 to 10% of HSV-1 or HSV-2 antigen-positive neurons were A5 positive and 13 to 16% were KH10 positive, suggesting that both viruses reach each type of neuron in a manner proportional to their representation in uninfected ganglia. In murine trigeminal ganglia harvested during HSV latency, 25% of HSV-1 latency-associated transcript (LAT)- and 4% of HSV-2 LAT-expressing neurons were A5 positive, while 12% of HSV-1 LAT- and 42% of HSV-2 LAT-expressing neurons were KH10 positive. A similar difference was observed in murine dorsal root ganglia. These differences could not be attributed to differences in LAT expression levels in A5- versus KH10-positive neurons. Thus, HSV-1 demonstrated a preference for the establishment of latency in A5-positive neurons, while HSV-2 demonstrated a preference for the establishment of latency in KH10-positive neurons. A chimeric HSV-2 mutant that expresses the HSV-1 LAT exhibited an HSV-1 phenotype, preferentially establishing latency in A5-positive neurons. These data imply that the HSV-1 and HSV-2 LAT regions influence the ability of virus to establish latency in different neuronal subtypes. That the same chimeric virus has a characteristic HSV-1 reactivation phenotype further suggests that LAT-influenced establishment of latency in specific neuronal subtypes could be an important part of the mechanism by which LAT influences viral reactivation phenotypes.

scholarly journals Recurrent Herpes Simplex Virus Type 1 (HSV-1) Infection Modulates Neuronal Aging Marks in In Vitro and In Vivo Models

2021 ◽  
Vol 22 (12) ◽  
pp. 6279
Author(s):  
Giorgia Napoletani ◽  
Virginia Protto ◽  
Maria Elena Marcocci ◽  
Lucia Nencioni ◽  
Anna Teresa Palamara ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Molecular Mechanisms ◽  
Neuronal Response ◽  
Viral Reactivation ◽  
In Vivo Models ◽  
Simplex Virus ◽  
Hsv 1

Herpes simplex virus 1 (HSV-1) is a widespread neurotropic virus establishing a life-long latent infection in neurons with periodic reactivations. Recent studies linked HSV-1 to neurodegenerative processes related to age-related disorders such as Alzheimer’s disease. Here, we explored whether recurrent HSV-1 infection might accelerate aging in neurons, focusing on peculiar marks of aged cells, such as the increase in histone H4 lysine (K) 16 acetylation (ac) (H4K16ac); the decrease of H3K56ac, and the modified expression of Sin3/HDAC1 and HIRA proteins. By exploiting both in vitro and in vivo models of recurrent HSV-1 infection, we found a significant increase in H4K16ac, Sin3, and HDAC1 levels, suggesting that the neuronal response to virus latency and reactivation includes the upregulation of these aging markers. On the contrary, we found a significant decrease in H3K56ac that was specifically linked to viral reactivation and apparently not related to aging-related markers. A complex modulation of HIRA expression and localization was found in the brain from HSV-1 infected mice suggesting a specific role of this protein in viral latency and reactivation. Overall, our results pointed out novel molecular mechanisms through which recurrent HSV-1 infection may affect neuronal aging, likely contributing to neurodegeneration.

Herpes simplex virus-1 oesophagitis presenting with persistent hiccough in an immunocompetent host: A case report

2021 ◽  
pp. 004947552110225
Author(s):  
Aritra Paul ◽  
Aruni Ghose
Keyword(s):  
Case Report ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Immunocompetent Host ◽  
Herpes Simplex Virus 1 ◽  
Diagnostic Work ◽  
Simplex Virus ◽  
Work Up ◽  
Diagnostic Work Up ◽  
Hsv 1

Herpes simplex virus-1 (HSV-1) oesophagitis as an aetiology of persistent hiccough is a rarity in immunocompetent hosts and entails an exhaustive diagnostic work-up, since it does not present with any of the typical oesophagitis symptoms. Our patient presented with persistent hiccoughs that were resistant to treatment with baclofen. Oesophagogastroduodenoscopy with biopsy confirmed the diagnosis of HSV-1 oesophagitis. The hiccough subsided within 48 h of aciclovir therapy.

scholarly journals Herpes Simplex Virus 1 Replication, Ocular Disease, and Reactivations from Latency Are Restricted Unilaterally after Inoculation of Virus into the Lip

2019 ◽  
Vol 93 (24) ◽  
Author(s):  
Nolwenn Poccardi ◽  
Antoine Rousseau ◽  
Oscar Haigh ◽  
Julie Takissian ◽  
Thierry Naas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Ocular Disease ◽  
Viral Reactivation ◽  
Trigeminal Ganglia ◽  
Herpes Simplex Virus 1 ◽  
Simplex Virus ◽  
Kinetics Of ◽  
Hsv 1

ABSTRACT Ocular herpes simplex keratitis (HSK) is a consequence of viral reactivations from trigeminal ganglia (TG) and occurs almost exclusively in the same eye in humans. In our murine oro-ocular (OO) model, herpes simplex virus 1 (HSV-1) inoculation in one side of the lip propagates virus to infect the ipsilateral TG. Replication here allows infection of the brainstem and infection of the contralateral TG. Interestingly, HSK was observed in our OO model only from the eye ipsilateral to the site of lip infection. Thus, unilateral restriction of HSV-1 may be due to differential kinetics of virus arrival in the ipsilateral versus contralateral TG. We inoculated mice with HSV-1 reporter viruses and then superinfected them to monitor changes in acute- and latent-phase gene expression in TG after superinfection compared to the control (single inoculation). Delaying superinfection by 4 days after initial right lip inoculation elicited failed superinfecting-virus gene expression and eliminated clinical signs of disease. Initial inoculation with thymidine kinase-deficient HSV-1 (TKdel) completely abolished reactivation of wild-type (WT) superinfecting virus from TG during the latent stage. In light of these seemingly failed infections, viral genome was detected in both TG. Our data demonstrate that inoculation of HSV-1 in the lip propagates virus to both TG, but with delay in reaching the TG contralateral to the side of lip infection. This delay is responsible for restricting viral replication to the ipsilateral TG, which abrogates ocular disease and viral reactivations from the contralateral side. These observations may help to understand why HSK is observed unilaterally in humans, and they provide insight into vaccine strategies to protect against HSK. IMPORTANCE Herpetic keratitis (HK) is the leading cause of blindness by an infectious agent in the developed world. This disease can occur after reactivation of herpes simplex virus 1 in the trigeminal ganglia, leading to dissemination of virus to, and infection of, the cornea. A clinical paradox is evidenced by the bilateral presence of latent viral genomes in both trigeminal ganglia, while for any given patient the disease is unilateral with recurrences in a single eye. Our study links the kinetics of early infection to unilateral disease phenomenon and demonstrates protection against viral reactivation when kinetics are exploited. Our results have direct implications in the understanding of human disease pathogenesis and immunotherapeutic strategies for the treatment of HK and viral reactivations.

scholarly journals Spontaneous Reactivation of Herpes Simplex Virus Type 1 in Latently Infected Murine Sensory Ganglia

2007 ◽  
Vol 81 (20) ◽  
pp. 11069-11074 ◽  
Author(s):  
Todd P. Margolis ◽  
Fred L. Elfman ◽  
David Leib ◽  
Nazzy Pakpour ◽  
Kathleen Apakupakul ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Infectious Virus ◽  
Viral Reactivation ◽  
Viral Shedding ◽  
Latently Infected ◽  
Simplex Virus ◽  
Spontaneous Reactivation ◽  
Hsv 1

ABSTRACT Careful studies of mouse trigeminal ganglia (TG) latently infected with herpes simplex virus type 1 (HSV-1) indicate the presence of productive cycle viral gene products and persistent immune response, suggesting ongoing spontaneous viral reactivation in these tissues. In the present study we set out to determine whether infectious virus is present in murine TG latently infected with HSV-1 (KOS). At 37 days after ocular inoculation we found a small amount of infectious virus in ca. 6% of latently infected murine TG. Furthermore, the amount of infectious virus that we detected (PFU per viral antigen-positive neuron) was similar to that detected in acutely infected ganglia. We conclude that spontaneous reactivation of infectious HSV-1 occurs in the mouse TG and is likely the principle cause of viral protein expression in these tissues. We next examined the role of latency-associated transcript (LAT) in spontaneous ganglionic reactivation by examining ganglia latently infected with KOS dlLAT1.8, a LAT deletion virus. Through the use of immunocytochemistry we found that KOS dlLAT1.8 had a rate of spontaneous ganglionic reactivation very similar to that of HSV-1 (KOS). Studying spontaneous ganglionic reactivation of HSV in the mouse TG allows a direct study of viral reactivation from latently infected neurons without the potential confounders and complicating downstream events that accompany the study of viral reactivation by explantation or peripheral viral shedding. Since most cases of human viral shedding and reactivation are not associated with a known trigger, spontaneous ganglionic reactivation of HSV-1 may be a better model of human disease than existing models.

Assembly of VP26 in herpes simplex virus-1 capsid implicated by 3-D structure of recombinant capsid

1995 ◽  
Vol 53 ◽  
pp. 840-841
Author(s):  
Z. Hong Zhou ◽  
Jing He ◽  
Joanita Jakana ◽  
J. D. Tatman ◽  
Frazer J. Rixon ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
3D Structure ◽  
Structure Study ◽  
Herpes Simplex Virus 1 ◽  
Shell Proteins ◽  
Life Threatening ◽  
Infected Cells ◽  
Simplex Virus ◽  
Hsv 1

Herpes simplex virus-1 (HSV-1) is a ubiquitous virus which is implicated in diseases ranging from self-curing cold sores to life-threatening infections. The 2500 Å diameter herpes virion is composed of a glycoprotein spike containing, lipid envelope, enclosing a protein layer (the tegument) in which is embedded the capsid (which contains the dsDNA genome). The B-, and A- and C-capsids, representing different morphogenetic stages in HSV-1 infected cells, are composed of 7, and 5 structural proteins respectively. The three capsid types are organized in similar T=16 icosahedral shells with 12 pentons, 150 hexons, and 320 connecting triplexes. Our previous 3D structure study at 26 Å revealed domain features of all these structural components and suggested probable locations for the outer shell proteins, VP5, VP26, VP19c and VP23. VP5 makes up most of both pentons and hexons. VP26 appeared to bind to the VP5 subunit in hexon but not to that in penton.

scholarly journals Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
David Shahnazaryan ◽  
Rana Khalil ◽  
Claire Wynne ◽  
Caroline A. Jefferies ◽  
Joan Ní Gabhann-Dromgoole ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Immune Responses ◽  
Tear Film ◽  
Cell Protein ◽  
Type I ◽  
Type I Ifn ◽  
Herpes Simplex Virus 1 ◽  
Simplex Virus ◽  
Hsv 1

AbstractHerpes simplex keratitis (HSK), caused by herpes simplex virus type 1 (HSV-1) infection, is the commonest cause of infectious blindness in the developed world. Following infection the virus is initially suspended in the tear film, where it encounters a multi-pronged immune response comprising enzymes, complement, immunoglobulins and crucially, a range of anti-viral and pro-inflammatory cytokines. However, given that HSV-1 can overcome innate immune responses to establish lifelong latency throughout a susceptible individual’s lifetime, there is significant interest in understanding the mechanisms employed by HSV-1 to downregulate the anti-viral type I interferon (IFN) mediated immune responses. This study aimed to investigate the interactions between infected cell protein (ICP)0 and key elements of the IFN pathway to identify possible novel targets that contribute to viral immune evasion. Reporter gene assays demonstrated the ability of ICP0 to inhibit type I IFN activity downstream of pathogen recognition receptors (PRRs) which are known to be involved in host antiviral defences. Further experiments identified interferon regulatory factor (IRF)7, a driver of type I IFN, as a potential target for ICP0. These findings increase our understanding of the pathogenesis of HSK and suggest IRF7 as a potential therapeutic target.

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