PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 16954297

Invader plus method detects herpes simplex virus in cerebrospinal fluid and simultaneously differentiates types 1 and 2.

Hatim T Allawi·Haijing Li·Tamara Sander·Azamat Aslanukov·Victor I Lyamichev·Amondrea Blackman·Slava Elagin·Yi-Wei Tang
View original source ↗Export metadata ↓

Abstract

We report here on the development and validation of a prototype Invader Plus method for the qualitative detection of herpes simplex virus types 1 and 2 in cerebrospinal fluid (CSF). The method combines PCR and Invader techniques in a single, closed-tube, continuous-reaction format that gives an analytical sensitivity of approximately 10 copies per reaction. The clinical sensitivity and specificity were 100.0% and 98.6%, respectively, when the results of the method were validated against the results obtained with a PCR colorimetric microtiter plate system by use of clinical CSF specimens.

Explore related subjects

Central Nervous System Viral DiseasesCerebrospinal FluidDNA ProbesDNA, ViralFluorescence Resonance Energy TransferHerpes SimplexHerpesvirus 1, HumanHerpesvirus 2, HumanPolymerase Chain ReactionSensitivity and SpecificityThymidine KinaseEvaluation StudyJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Hatim T Allawi, Haijing Li, Tamara Sander, Azamat Aslanukov, Victor I Lyamichev, Amondrea Blackman, Slava Elagin, Yi-Wei Tang. 2006. Invader plus method detects herpes simplex virus in cerebrospinal fluid and simultaneously differentiates types 1 and 2.. https://doi.org/10.1128/jcm.01175-06

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2005

Macrophages and HIV-1: dangerous liaisons.

HIV-1, like the other lentiviruses, has evolved the ability to infect nondividing cells including macrophages. HIV-1 replication in monocytes/macrophages entails peculiar features and differs in many respects from that in CD4 T lymphocytes. HIV-1 exhibits different tropism for CD4 T cells and macrophages. The virus can enter macrophages via several routes. Mitosis is not required for nuclear import of viral DNA or for its integration into the host cell genome. Specific cellular factors are required for HIV-1 transcription in macrophages. The assembly and budding of viral particles in macrophages take place in late endosomal compartments. Viral particles can use the exosome pathway to exit cells. Given their functions in host defence against pathogens and the regulation of the immune response plus their permissivity to HIV-1 infection, monocytes/macrophages exert a dual role in HIV infection. They contribute to the establishment and persistence of HIV-1 infection, and may activate surrounding T cells favouring their infection. Furthermore, monocytes/macrophages act as a Trojan horse to transmit HIV-1 to the central nervous system. They also exhibit antiviral activity and express many molecules that inhibit HIV-1 replication. Activated microglia and macrophages may also exert a neurotrophic and neuroprotective effect on infected brain regulating glutamate metabolism or by secretion of neurotrophins. This review will discuss specific aspects of viral replication in monocytes/macrophages and the role of their interactions with the cellular environment in HIV-1 infection swinging between protection and pathogenesis.

Central Nervous System Viral Diseases↗
PubMed2005

Human herpesviruses-6 and -7 infections.

PURPOSE OF REVIEW: To summarize the biology and clinical consequences of infection with the closely related human herpesviruses-6 and -7 (HHV-6/7) in children. RECENT FINDINGS: Over the last year there has been a paucity of paediatric publications on HHV-6 and only two studies focused on HHV-7. Steady progress has been made regarding the biology and clinical consequences of HHV-6 infection whereas the effect of HHV-7 infection remains a neglected topic. However, both viruses have been shown to contribute significantly and equally to the burden of disease in young children with suspected encephalitis or severe convulsions with fever. There continues to be uncertainty as to the effects of HHV-6 infection after stem cell transplant, although there is general agreement that it contributes to encephalitis. In contrast, HHV-7 seems to have little clinical impact after stem cell transplant, although central nervous system infection and disease have recently been reported in children. Understanding the contribution of chromosomal integration and inheritance of both HHV-6 variants A and B (HHV-6A/B) and their effect on diagnosis is emerging. SUMMARY: There is an urgent need for more research on HHV-6 and -7 in children, particularly in relation to chromosomal integration of HHV-6A and B, and clinical consequences of HHV-7 infection.

Central Nervous System Viral Diseases↗