Herpes simplex virus (HSV) infections are common and widespread; nevertheless, their outcome can be of unpredictable prognosis in neonates and in immunosuppressed patients. Anti-HSV therapy is effective, but the emergence of drug-resistant strains or the drug toxicity that hamper the treatment is of great concern. Vaccine has not yet shown relevant benefit; therefore, palliative prophylactic measures have been adopted to prevent diseases. This short review proposes to present concisely the history of HSV, its taxonomy, physical structure, and replication and to explore the pathogenesis of the infection, clinical manifestations, laboratory diagnosis, treatment, prophylaxis and epidemiology of the diseases.
- MeSH
- antivirové látky terapeutické užití MeSH
- herpes genitalis diagnóza farmakoterapie epidemiologie imunologie MeSH
- herpes simplex diagnóza farmakoterapie epidemiologie imunologie MeSH
- imunokompromitovaný pacient MeSH
- lidé MeSH
- lidský herpesvirus 1 klasifikace účinky léků růst a vývoj patogenita MeSH
- lidský herpesvirus 2 klasifikace účinky léků růst a vývoj patogenita MeSH
- novorozenec MeSH
- replikace viru účinky léků genetika MeSH
- Check Tag
- lidé MeSH
- novorozenec MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- antivirové látky MeSH
Varicella-zoster virus (VZV), herpes simplex virus one (HSV-1) and herpes simplex virus two (HSV-2) represent three out of the eight known human herpesviruses and belong to the subfamily of α-herpesviruses. These viruses are present worldwide and humans are their sole host and reservoir. After the primary infection, these viruses persist in the body throughout life. The period of latency may be interrupted by reactivation of infection due to various factors. Each virus can induce a wide spectrum of diseases. The primary infection is typical for children and otherwise healthy individuals are often asymptomatic. It is mainly immunocompromised patients who are at risk of developing severe disease or complications when infected by these viruses. However, even in otherwise healthy individuals an infection by a-herpesviruses can run a severe course and lead to death.
- MeSH
- herpetické infekce epidemiologie virologie MeSH
- imunokompromitovaný pacient MeSH
- lidé MeSH
- lidský herpesvirus 1 klasifikace genetika izolace a purifikace MeSH
- lidský herpesvirus 2 klasifikace genetika izolace a purifikace MeSH
- virus varicella zoster klasifikace genetika izolace a purifikace MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Česká republika epidemiologie MeSH
The genetic background of HSZP virus, an HSV1 strain with extensive passage history, was analyzed by parallel comparative sequencing of four relevant genes (UL27/gB, UL41/vhs, UL44/gC and UL53/gK) of HSZP and additional three selected viruses [strains ANGpath, strains KOS(a) and KOS(b) and the prototype strain 17]. Mutation at position 858 (His for Arg) in gB of HSZP was found to be responsible for giant cell formation (syn3gB mutation) similarly as the 855 mutation (Val for Ala) in the gB of ANGpath. No syn1gK mutations were detected in the UL53 gene either of HSZP or of ANGpath viruses. The reduced virulence of HSZP for adult mice after peripheral inoculation, similarly as that of KOS virus, seems to be related (at least in part) to numerous mutations in the gB ectodomain. Of these, two mutations located in the antigenic domain IV were the same in gBHSZP as well as in gBKOS (at amino acids 59 and 79), at least two (amino acids 313 and 553) were specific for gBKOS, while one mutation (Ser for Ala at position 108) was specific for gBHSZP. The abolished shutoff function of the HSZP virus was related to at least four out of six specific mutations seen in the vhs polypeptide (vhsHSZP) encoded by the UL41 gene, of which three (amino acids 374, 386, 392) were clustered in the semiconservative box A of vhsHSZP (the truncation of which abrogates the inhibition provided by this protein) and one mutation (at amino acid 18) was situated in the highly conservative locus I of vhsHSZP. In addition, the two vhsKOS specific mutations (amino acids 19 and 317) not found in vhsHSZP, enhanced the early host shutoff function of the vhsKOS protein. Finally, gCHSZP had two specific mutations (amino acids 137 and 147) located in the antigenic domain II of gC, which is responsible for binding of HSV1 virions to the glycosoaminoglycan (GAG) receptor. When expressed in Sf21 cells using the recombinant baculovirus system (Bac-to-Bac), gCHSZP and gCKOS showed no essential antigenic differences.
- MeSH
- antigeny virové chemie genetika MeSH
- druhová specificita MeSH
- králíci MeSH
- kuřecí embryo MeSH
- lidský herpesvirus 1 klasifikace genetika patogenita MeSH
- mutace MeSH
- myši MeSH
- proteiny virového obalu chemie genetika imunologie MeSH
- sekvence aminokyselin MeSH
- terciární struktura proteinů MeSH
- virové geny MeSH
- virulence genetika MeSH
- zvířata MeSH
- Check Tag
- králíci MeSH
- kuřecí embryo MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antigeny virové MeSH
- glycoprotein B, Simplexvirus MeSH Prohlížeč
- proteiny virového obalu MeSH