Varicella zoster virus vs herpes simplex virus

Twenty-four hours after electroporation, supernatants were collected and analyzed using the cytotoxicity assay. To investigate the way in which HS3ST4 contributes to viral genome replication, we analyzed copy numbers of the viral genome chronologically.

These results suggested that the expression of HS3ST4 had little effect on viral genome replication. Based on these associations, we investigated the contribution of HS3ST4 to virus-induced cytopathology and viral replication using human MeWo cells. Introns occasionally function to regulate transcription. From these data, it can be easily speculated that in individuals who exhibit more robust HS3ST4 expression, reactivated VZV may more easily trigger disease pathogenesis. However, further studies are needed to prove the function of this SNP including the correlation among the genotypes of the SNP, the expression levels of HS3ST4, and the intensity of cell fusion in vivo.

VZV-infected MeWo cells fuse with the human neuronal somata. Thus, neuronal cell fusion after VZV infection can be observed in humans. Further studies are needed to investigate this possibility.

Hyperfusogenic measles virus and other paramyxovirus mutants induced strong cytopathology through cell fusion in infected cells, despite the suppression of viral replication. In the present study, we assayed cell fusion using human cells that are naturally susceptible to VZV. This modification of HS in receptors on the cell surface would promote cell-cell attachment, followed by cell fusion.

We thank Mr Michael Arends for editing the manuscript. We are grateful to the volunteers for their participation in the study and anesthesiologists and surgeons for collecting the clinical data. Formal analysis: Seii Ohka. Investigation: Seii Ohka, Kazutaka Ikeda. Project administration: Seii Ohka, Kazutaka Ikeda. Validation: Seii Ohka. Visualization: Seii Ohka.

Writing-original draft preparation: Seii Ohka. Supplemental Material: Supplemental material for this article is available online. National Center for Biotechnology Information , U. Journal List Mol Pain v. Mol Pain.

Published online Dec Author information Article notes Copyright and License information Disclaimer. Email: pj. Associated Data Supplementary Materials sj-xlsxmpx Abstract Acute pain that is associated with herpes zoster HZ can become long-lasting neuropathic pain, known as chronic post-herpetic neuralgia PHN , especially in the elderly. Keywords: post-herpetic neuralgia, neuropathic pain, varicella-zoster virus, herpes zoster, single-nucleotide polymorphism, heparan sulfate 3- O -sulfotransferase 4, glycoproteins, fusogenic activity.

Introduction Post-herpetic neuralgia PHN is long-lasting neuropathic pain that is caused by the reactivation of latent varicella-zoster virus VZV; i. Materials and methods Human genetic association analysis of genome-wide genotyping data Subjects with chronic pain and healthy subjects: The human GWAS was performed in our previous study.

Virus The VZV wildtype strain , which was isolated in our laboratory from the blister contents of a 9-year-old girl with HZ, was used in this study. Open in a separate window. Figure 3. Table 1. Table 2. Figure 1. Figure 2. Higher cytotoxicity in cells with HS3ST4 after infection To quantitatively determine the time course of cell fusion after infection, cells with and without HS3ST4 were infected or mock-infected with VZV, and supernatants were collected on each day after infection and analyzed using the cytotoxicity assay Supplementary Dataset S2.

Figure 4. Figure 5. Figure 6. VZV genome replication had similar efficiency in the cells with HS3ST4 To investigate the way in which HS3ST4 contributes to viral genome replication, we analyzed copy numbers of the viral genome chronologically. Figure 7. Supplemental Material sj-xlsxmpx Acknowledgments We thank Mr Michael Arends for editing the manuscript. References 1. Varicella-zoster virus glycoproteins: Entry, replication, and pathogenesis. Curr Clin Microbiol Rep ; 3 : — Genome-wide association study identifies candidate loci associated with chronic pain and postherpetic neuralgia.

Mol Pain ; 17 : Ulceration and crusting of lesions, with ultimate resolution, typically occurs in 2 to 6 weeks in immunocompetent patients; however, lesions may persist much longer in immunocompromised patients, such as those with HIV.

For orolabial herpes Figure 1 , mouth buccal and gingival mucosa and lips are the most common sites. Recurrent lesions are commonly found on the vermilion border. Other sites may include perioral skin, nasal mucosa, and hard palate. Primary genital herpes can produce erosive balanitis, vulvitis, or vaginitis.

In women, lesions can also involve the cervix, buttocks, and perineum. In men, lesions most often occur on the penile shaft or glans Figure 2 ; recurrent lesions may occur on the genitals or buttocks and resolve within 1 week. Frequency of recurrent lesions may be related to the severity of the primary infection. In patients with HIV, lesions may lead to deep ulcerations around the nose, mouth, genitals, and even distal fingers Figure 3, Figure 4, Figure 5.

Verrucous or tumor-like lesions have been reported Figure 6. Genital Herpes Simplex: After the vesicles have ruptured, patients may manifest with an ulcer with a scalloped border. Herpes simplex virus HSV can be spread by infected individuals who are asymptomatic or symptomatic during times of viral shedding. HSV-1, which is more commonly associated with oral herpes, is primarily spread by contact with infected saliva or other secretions. HSV-2, which is more commonly associated with genital herpes, is primarily spread by sexual contact.

The virus replicates at the site of infection, travels retrograde to the dorsal root ganglion, and establishes latent infection. Recurrent lesions occur with reactivation of latent disease. Triggers for reactivation of latent disease include stress, fever, immunocompromised state, damage to local tissue, and ultraviolet light.

Risk factors for acquiring genital disease are age 15 to 30 years, increased number of sexual partners, black or Hispanic race, and HIV positivity. Varicella zoster virus infection: Individual lesions of varicella zoster may look exactly like herpes simplex, with clustered vesicles or ulcers on an erythematous base. Varicella zoster tends to follow a dermatomal distribution, which can help to distinguish from herpes simplex.

Disseminated herpes simplex and disseminated zoster may be indistinguishable clinically. Aphthous ulcers: These occur most commonly in the mouth but can also involve the genitals, such as in Behcet disease.

Large aphthous ulcers can be associated with HIV infection. These most commonly occur on the mucosal inner lips, tongue, floor of the mouth, and inner cheeks. They occur as small round ulcers with a yellow or grey ulcer floor, which often occur singly or in a linear fashion. They usually heal within 1 week. HIV infection: HIV may present with major aphthous ulcerations, which occur most commonly on the oral mucosa.

Serologic tests can show primary seroconversion for HSV-1 or HSV-2 infection; however, it does not definitively diagnose active disease.

Tzank smear: Scraping of the base of an early unroofed blister can demonstrate virally infected multinucleated epithelial giant cells. Viral tissue culture: This may be positive within 48 hours and can allow for resistance testing if needed. HSV deoxyribonucleic acid detection: Gene amplification by PCR, ligase chain reaction, or other methods can be done on skin lesions or cerebral spinal fluid when evaluating for encephalitis and other infected tissue.

Direct fluorescent antibody: Cells scraped from the base of an early unroofed blister are stained with a direct fluorescent antibody. Imaging studies are only useful when there is suspected HSV encephalitis. Brain imaging studies, such as computed tomography and magnetic resonance imaging scans, can be performed to look for involvement of the temporal lobe. If you decide the patient has herpes simplex virus infection, what therapies should you initiate immediately?

Dermatology would be most helpful in diagnosing this infection when there is skin or mucous membrane involvement. If the patients are immunocompetent, no therapy may be necessary since the lesions usually self-resolve. If the patient is immunocompromised, severely symptomatic, or disseminated or the lesions are extensive, treatment is needed. The most common specimens from immunocompromised patients that are analyzed for detection of herpes simplex virus HSV or varicella-zoster virus VZV are from skin lesions.

Many types of assays are applicable to these samples, but some, such as virus isolation and direct fluorescent antibody testing, are useful only in the early phases of the lesions. In contrast, nucleic acid NA detection methods, which generally have superior sensitivity and specificity, can be applied to skin lesions at any stage of progression.