• Toxicological Research
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• 제4권1호
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• pp.47-53
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• 1988

Cholera toxin and dibutyryl cyclic adenosine 3', 5'-monophosphate(db-cAMP) increased the rate and number of infections units produced in the in vitro reactivation of latent herpes simplex virus, whereas adenosine diminished them. cAMP concentration in latently infected trigeminal ganglia of mice was greatly increased by cholera toxin but was not affected by adenosine.

• 대한치과의사협회지
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• 제48권5호
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• pp.365-370
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• 2010

Herpes virus family is highly infectious to patients, their families and dentists. The diagnosis of herpes infection is based on the characteristic clinical appearance and the location of the lesions. Herpes Simplex Virus(HSV) usually acquired through direct contact with infected lesions or body fluids, and the prevalence of HSV infection increases progressively from childhood. Primary infections provoke herpetic gingivostomatis typically affects the tongue, lips, gingival, buccal mucosa and palate. Recurrent infections give rise to vesiculo-ulcerative lesions at vermilion border of lip(herpes labialis). In the form of chickenpox, Varicella Zoster Virus(VZV) usually is infected in childhood. VZV spreads in the affected primary afferent nerve to the skin and produces a vesicular rash and pain. Epstein-Barr Virus(EBV) infects B cells and cause infectious mononucleosis. Latent EBV infection has also been implicated in Burkitt lymphoma, nasopharyngeal carcinoma. Cytomegalovirus(CMV) is associated with immune-compromised patient such as organ transplantation and AIDS patients.

• 대한약리학회지
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• 제22권2호
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• pp.123-127
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• 1986

4-carbon fatty acid인 n-Butyrate(n-BTA)는 herpes virus의 일종인 Epstein-Bat virus(EBV)에 작용해서 잠복형인 EBV를 활성형태로 유도시키는 것으로 알려져 있다. 고로 본 실험에서는 mouse의 삼차신경절에 잠복하고 있는 HSV의 재활성화에 대한 n-BTA의 효과를 실험 관찰하였다. Pentobarbital로 마취시킨 mouse의 양쪽눈 각막을 30 gauge 주사바늘로 scarify한 후에 type I HSV(HSV-1) $10{\mu}1(1{\times}10^5$ plaque-forming units)를 각각 점안 감염시켰다. virus를 감염시킨 4주 후에 mouse의 삼차신경절을 적출하여 시험관 내에서 조직배양을 시행하였다. 조직배양시에 0. 1, 0. 25, 0.5. 1.0 그리고 2.0mM농도의 n-BTA를 첨가하였으며 1일, 2일, 3일간 각각 배양한 후 신경절을 연마하여 연마액내의 HSV-1 titer를Vero cell monolayer에서 plaque assay로 측정하였다. 1) n-BTA첨가군은 잠재성 HSV가 대조군에 비하여 현저하게 빨리 재활성화 되었고 재활성화되는 virus의 양도 현저히 증가되었다. 2) 24시간을 계속해서 n-BTA 각 농도를 첨가해서 배양할 군은 n-BTA 6시간 첨가 배양하고 새로운 배양액으로 갈아서 18시간 배양한 군에 비해 잠재성 virus의 재활성화가 현저히 증가되었다. 3) Gang1ionic latent HSV-1의 재 활성화에 영향을 미치는 각 농도의 n-BTA는 Vero cell의 monolayer에서의 HSV-1의 번식에는 아무런 영향을 미치지 않았다.

• 대한바이러스학회지
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• 제30권3호
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• pp.171-178
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• 2000

Herpes simplex virus, Varicella zoster virus and Human herpes virus-6 caused central nervous system infections and latent infections but there is no data of the 3 viruses being tested from the same cerebrospinal fluid samples with aseptic meningitis or encephalitis in adults patients. These viruses produced similar neurologic symptoms but difficulties existed in differentiating of etiologic agents and therefore the viruses needed to be detected in the early state. Herpes simplex virus encephalitis (HSVE) in adults, if not treated promptly was fatal. If treated with antiviral drugs in the early phase of encephalitis, neurologic sequales decreased by 65%. Recently, a PCR method for detection of HSVE with CSF was developed. VZV primary and secondary infections caused neurologic symptoms of encephalitis or meningitis. The second frequency of adult encephalitis that caused VZV were reported. HHV-6 caused CNS latent infection that was studied with normal adults brains. But there is no data of HSV, VZV and HHV-6 for aseptic meningitis and encephalitis of Korean adults through etiologic study. We cultured CSFs on HEp-2 cells and simultaneously tested for HSV PCR, VZV nested PCR and HHV-6 PCR with 8 specific primers. The PCR results of CSF from meningitis Korean adults were 13/19 (68.4%) for HSV, 10/19 (52.6%) for VZV and 12/19 (63.2%) for HHV-67/19 (36.8%) cases were triple infected HSV PCR, VZV PCR and HHV-6 PCR positive; 3/19 (15.8%) cases were dual infected HSV PCR and HHV-6 PCR positive; 1119 (0.5%) cases was VZV PCR positive. Strong viral DNA amplification of CSF means a causative virus may be present in aseptic meningitis or encephalitis patients and may cause clinical neurologic symptoms. HSV and HHV-6 viruses detection rate were higher than VZV by PCR with CSFs.

• IMMUNE NETWORK
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• 제14권4호
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• pp.187-200
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• 2014

Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are the most common cause of genital ulceration in humans worldwide. Typically, HSV-1 and 2 infections via mucosal route result in a lifelong latent infection after peripheral replication in mucosal tissues, thereby providing potential transmission to neighbor hosts in response to reactivation. To break the transmission cycle, immunoprophylactics and therapeutic strategies must be focused on prevention of infection or reduction of infectivity at mucosal sites. Currently, our understanding of the immune responses against mucosal infection of HSV remains intricate and involves a balance between innate signaling pathways and the adaptive immune responses. Numerous studies have demonstrated that HSV mucosal infection induces type I interferons (IFN) via recognition of Toll-like receptors (TLRs) and activates multiple immune cell populations, including NK cells, conventional dendritic cells (DCs), and plasmacytoid DCs. This innate immune response is required not only for the early control of viral replication at mucosal sites, but also for establishing adaptive immune responses against HSV antigens. Although the contribution of humoral immune response is controversial, $CD4^+$ Th1 T cells producing IFN-${\gamma}$ are believed to play an important role in eradicating virus from the hosts. In addition, the recent experimental successes of immunoprophylactic and therapeutic compounds that enhance resistance and/or reduce viral burden at mucosal sites have accumulated. This review focuses on attempts to modulate innate and adaptive immunity against HSV mucosal infection for the development of prophylactic and therapeutic strategies. Notably, cells involved in innate immune regulations appear to shape adaptive immune responses. Thus, we summarized the current evidence of various immune mediators in response to mucosal HSV infection, focusing on the importance of innate immune responses.