Quantification of Feline Herpesvirus 1 DNA in Ocular Fluid Samples of Clinically Diseased Cats by Real-Time TaqMan PCR

Vögtlin, Andrea; Fraefel, Cornel; Albini, Sarah; Leutenegger, Christian M.; Schraner, Elisabeth M.; Spiess, Bernhard M.; Lutz, Hans; Ackermann, Mathias

doi:10.1128/jcm.40.2.519-523.2002

Cited by 91 publications

(93 citation statements)

References 24 publications

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“…PCR, which targets specific regions of the genome, demonstrates that viral DNA is present in the swab, rather than the presence of infectious virus. PCR is generally more sensitive than virus isolation, detecting virus for longer in the acute stages of the disease, and in more chronic stages [124,125,131,141,146]. However, a comparison of the various PCR tests available does show considerable differences in sensitivity between the published tests [83].…”

Section: Diagnosismentioning

confidence: 99%

“…shed virus under natural conditions, and even then, transmission to susceptible animals is not necessarily easily achieved [30,34]. More recent studies using PCR, including realtime PCR, have shown a higher sensitivity for detecting carriers, with a more prolonged presence of viral DNA in the secretions of infected cats [8,45,83,111,125,131,141,146,147]. Whilst such molecular techniques help identify carriers, the epidemiological significance of cats in which viral genome can be detected by PCR, but from which infectious virus cannot be isolated is not clear, as transmission studies have not been performed.…”

Section: Epidemiologymentioning

confidence: 99%

“…Infectious virus can be detected in oropharyngeal and nasal swabs as early as 24 h after infection and generally persists for 1 to 3 weeks, although viral DNA may be detected by PCR for longer [141,146].…”

Section: Pathogenesismentioning

confidence: 99%

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Feline herpesvirus

et al. 2007

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Section: Diagnosismentioning

confidence: 99%

Section: Epidemiologymentioning

confidence: 99%

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Feline herpesvirus

et al. 2007

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“…Signals were regarded as positive if the fluorescence intensity exceeded 10 times the standard deviation of the baseline fluorescence (threshold cycle, ct). The sensitivity and specificity of the system were determined essentially as described before for ovine herpesvirus 2 and feline herpesvirus 1 (26,42).…”

Section: Methodsmentioning

confidence: 99%

Both Viral and Host Factors Contribute to Neurovirulence of Bovine Herpesviruses 1 and 5 in Interferon Receptor-Deficient Mice

Abril

Engels

Liman

et al. 2004

J Virol

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Herpes simplex virus (HSV) type 1 and bovine herpesviruses 1 and 5 (BHV-1 and BHV-5) can use the same cellular receptor for entry, but only HSV is known to cause disease in mice. We hypothesized that components of either the innate or the adaptive immune system, or a combination of both, were responsible for curbing replication of BHVs in mice. Therefore, wild-type mice as well as mice with various combined genetic deficiencies in the alpha/beta interferon receptor or gamma interferon receptor and in the ability to produce mature B and T lymphocytes (RAG-2 deletion) were infected with BHV-1 and BHV-5 and monitored clinically, serologically, histopathologically, and virologically. A functional immune system protected the mice from disease and death due to BHV infection, and the immune response was Th1 like. BHV-5 was transported to the central nervous system by the axonal pathway, whereas viremia was required for this outcome with BHV-1. The alpha/beta interferon system was able to obstruct quantitative spread of the viruses in the infected organism. The gamma interferon system had a protective effect against BHV-1, even in mice with the RAG-2 deletion. In contrast, the same mice succumbed to neurological disease and death upon infection with BHV-5. Productively infected neurons were detected only in BHV-5-infected mice with an intact gamma interferon system. We conclude that the alpha/beta interferon system had a protective effect, while an intact gamma interferon system was required for efficient replication of BHV-5 in mouse neurons and for the development of neurological disease.

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“…With the exception of total urine and urine supernatant, the DNA of all of the different samples was extracted by a QIAamp DNA Mini kit (Qiagen, Basel, Switzerland). Carrier DNA (50 g of salmon sperm DNA/ml; Life Technologies AG, Basel, Switzerland) was added to the elution buffer (AE) to elute the DNA of the semen samples (22). As suggested by the manufacturer, the QIAamp Viral RNA Mini kit containing a special buffer (AVL) was used to extract the DNA of total urine and the supernatant.…”

Section: Methodsmentioning

confidence: 99%

Analysis of the Pathogenetic Basis for Shedding and Transmission of Ovine Gamma Herpesvirus 2

et al. 2002

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Ovine herpesvirus 2 (OvHV-2), a member of the viral subfamily Gammaherpesvirinae, shares numerous similarities with human herpesvirus 8 (HHV-8). Both viruses are apathogenic in their healthy original host, may cause lymphoprolipherative diseases, cannot routinely be propagated in cell culture, and may be sexually transmitted. However, the pathways of sexual transmission of these viruses, as well as the underlying pathogenetic dynamics, are not well understood. Organs from naturally OvHV-2-infected, as well as OvHV-2-free, sheep were quantitatively analyzed for OvHV-2 by the DNA amplification techniques. The dynamics of OvHV-2 multiplication and excretion were monitored after experimental infections and, most importantly, subsequent to vasectomy. The OvHV-2 DNA load in various tissues and internal organs was not merely reflecting the viral DNA load in the bloodstream, which suggested compartmentalization of OvHV-2. Moreover, OvHV-2 DNA was detected at several portals for virus shedding, i.e., the respiratory, alimentary, and urogenital tracts. Transient OvHV-2 excretion was detected in ejaculates of experimentally infected rams. Upon vasectomy, OvHV-2 DNA reappeared in the ejaculatory plasma, but the titers did not decline after reaching a peak. Spiking and fractionation experiments revealed an inhibitory activity, associated with the spermatozoa, which was able to suppress detection of viral DNA but which was no longer present in samples from vasectomized animals. Therefore, epidemiological studies on viruses that may be transmitted by the ejaculatory pathway and for whose tracing nucleic acid amplification methods are used, i.e., OvHV-2, HHV-8, and the human immunodeficiency virus, should include vasectomized males.The hallmarks of gamma herpesviruses, i.e., ovine herpesvirus 2 (OvHV-2; the causative agent of malignant catarrhal fever) and the tumorigenic human herpesvirus 8 (HHV-8), include restricted host range and causing host-specific, proliferative, immunopathological diseases (13,15,19). HHV-8 and OvHV-2 share at least three important features:(i) Normally, they are not associated with disease in the healthy original host. However, in the immunologically ill adapted host, they are causative agents of lymphoproliferative diseases. (ii) Natural isolates cannot routinely be propagated in cell culture (7,18). Therefore, efficient tracing of these viruses relies on DNA amplification techniques. (iii) Several lines of evidence suggest that they may be sexually transmitted (2, 3, 14, 16). However, the reported prevalences of HHV-8 in prostate and semen range from zero to Ͼ90% (reviewed in reference 9). To date, hardly any information concerning the pathogenesis and shedding of OvHV-2 has been presented.Good animal models for studying HHV-8 infections are not available (4). However, specific-OvHV-2-free sheep may be employed to gain significant information on infection, pathogenesis, and transmission of gammaherpesviruses.To gain insight into the pathogenetic basis for gammaherpesvirus excretion, organs from natu...

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Quantification of Feline Herpesvirus 1 DNA in Ocular Fluid Samples of Clinically Diseased Cats by Real-Time TaqMan PCR

Cited by 91 publications

References 24 publications

Feline herpesvirus

Feline herpesvirus

Both Viral and Host Factors Contribute to Neurovirulence of Bovine Herpesviruses 1 and 5 in Interferon Receptor-Deficient Mice

Analysis of the Pathogenetic Basis for Shedding and Transmission of Ovine Gamma Herpesvirus 2

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