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PubMedDate not supplied

Effect of oral acyclovir treatment on symptomatic and asymptomatic virus shedding in recurrent genital herpes.

Twenty-six men and women with recurrent genital herpes maintained diaries of their symptoms and signs of infection and submitted 6,515 self-collected cultures during a one-year study of acyclovir therapy. As compared with periods before or after treatment, the mean rates of experiencing symptoms or lesions, and of shedding virus were significantly lower during treatment. Acyclovir treatment reduced the rate of symptomatic shedding from 95 positive cultures to six per 1,000 cultures, but the rate of asymptomatic shedding remained relatively constant, averaging eight per 1,000 cultures. Among the isolates of herpes simplex virus studied, there was no differences in sensitivity to acyclovir between strains recovered on or off therapy or during symptomatic or asymptomatic recurrences. The endonuclease cleavage profiles of asymptomatically shed viruses were essentially the same as those of the symptomatically shed viruses from the same individual. Chronic acyclovir therapy significantly reduced the symptoms and signs of recurrent genital herpes but did not eliminate virus shedding, nor, therefore, the possibility of disease transmission.

Acyclovir↗
PubMed2001

Prolonged measles virus shedding in human immunodeficiency virus-infected children, detected by reverse transcriptase-polymerase chain reaction.

A reverse transcriptase-polymerase chain reaction assay was used to detect measles virus RNA in peripheral blood mononuclear cells, urine, and nasopharyngeal specimens from Zambian children during hospitalization and approximately 1-2 months after discharge. Of 47 children, 29 (61.7%) had prolonged measles virus shedding, as defined by detection of measles virus RNA in > or =1 specimen obtained 30-61 days after rash onset. Ten (90.9%) of 11 human immunodeficiency virus (HIV)-infected children had prolonged measles virus shedding, compared with 19 (52.8%) of 36 HIV-uninfected children (P=.02). Prolonged measles virus shedding did not correlate with levels of measles virus-specific antibody. HIV-infected children with measles may have a prolonged infectious period that potentially enhances measles virus transmission and hinders measles control.

Adolescent↗
PubMed2004

Lack of evidence of measles virus shedding in people with inapparent measles virus infections.

Serological evidence of measles virus infection has been detected among people exposed to measles who do not exhibit classical clinical symptoms. Throat swabs, lymphocytes, and serum and urine samples were collected from contacts of individuals with confirmed measles 12-16 days after exposure, during measles outbreaks occurring in 1998. Follow-up serum samples were drawn 2 weeks later. Samples were tested for measles IgM antibody by enzyme immunoassays and plaque reduction neutralization testing. Virus isolation and reverse transcriptase-polymerase chain reaction testing was attempted for all samples. None of the 133 contacts developed classical measles disease; 11 (8%) had serological evidence of infection. Duration of exposure of >or=3 h was the only significant risk factor for developing serological response (24% vs. 4% among contacts exposed for 1-2 h; relative risk, 6.0; 95% confidence interval, 1.9-19.2). None of the 133 contacts had virological evidence of infection by culture or polymerase chain reaction. We found no evidence that persons with inapparent measles virus infections shed measles virus.

Adolescent↗
PubMed2001

Herpes simplex virus shedding and plasma human immunodeficiency virus RNA levels in coinfected women.

Asymptomatic herpes simplex virus (HSV) shedding was described in a cohort of human immunodeficiency virus (HIV)-infected women, and the association of HSV shedding with changes in plasma HIV RNA load was investigated. Genital, rectal, and oral swabs were obtained daily during a 4-week period for polymerase chain reaction and culture, and concomitant plasma specimens were drawn 3 times weekly for determination of HIV RNA load. During the study, 70% and 79% of subjects shed HSV from the oral cavity and genital area, respectively. Shedding of HSV occurred for a mean of 3.2 days for oral shedding and 5.4 days for genital shedding. Mean plasma HIV RNA loads during periods of HSV shedding and nonshedding and for periods 3 days after the cessation of shedding were compared; no significant differences were found (P=.74). In women who shed HSV, as evaluated by detection of virus, plasma HIV RNA load did not fluctuate with HSV shedding.

Case-Control Studies↗
PubMed1998

Herpes simplex virus shedding among human immunodeficiency virus-negative men who have sex with men: site and frequency of shedding.

The frequency and anatomic location of subclinical and symptomatic herpes simplex virus (HSV) shedding were evaluated among human immunodeficiency virus (HIV)-negative HSV-2-seropositive men who have sex with men (MSM). Eight men attended a research clinic daily for 30 days for a detailed genital examination and anoscopy with colposcopy to detect herpes lesions. HSV cultures were obtained daily from four sites (perianal, urethral, penile shaft, and oral) at home and the research clinic. Signs and symptoms of genital herpes were recorded by the participants and clinician. Three (37.5%) of the men shed HSV. Overall, the 8 men shed HSV on 5.5% of days cultures were obtained and shed subclinically on 2.7% of days. All HSV shedding was perianal or rectal; only 1 symptomatic recurrence, concurrent with an external perianal lesion, was detected by anoscopy. Subclinical HSV shedding was frequent among HIV-negative MSM, and anoscopy with colposcopy did not increase the detection rate of rectal HSV lesions or shedding.

Adult↗
PubMed1984

Rotavirus carriage, asymptomatic infection, and disease in the first two years of life. I. Virus shedding.

From September 1979 to July 1980 inclusive, rotaviruses were prospectively detected by electron microscopy (EM) and ELISA in 82 (29%) of 283 children under two years of age who were admitted to a general pediatric ward in Paris. Rotavirus was found in 43 (36%) of 119 children with diarrhea and in 40 (24%) of 164 children without diarrhea; thus of 83 children shedding rotavirus, 40 (48%) were not diarrheic. Virus shedding that was not associated with diarrhea was observed in 71% of neonates, in 50% of one- to six-month-old children, and in 26% of 7-24-month-old children. Rotavirus shedding was statistically correlated (P less than .01) only with those cases of diarrhea with fever and vomiting ( DFV syndrome). Consequently, relative risk (RR) for the DFV syndrome in patients who were shedding virus was 2.07 (P less than .001) vs. 0.95 for other types of diarrhea. These observations show that asymptomatic rotaviral infection is not an infrequent occurrence; that the association between rotavirus and diarrhea is not necessarily an etiologic one; and that the DFV syndrome appears as a major clinical expression of rotaviral disease. Consequently, recovery of rotavirus from feces is of little diagnostic significance since it does not give a differentiation between rotavirus-induced and rotavirus-associated diarrhea.

Aging↗
PubMed2005

Application of a molecular panel to demonstrate enterotropic virus shedding by healthy and human immunodeficiency virus-infected patients.

We used a molecular panel, targeting seven enteric viruses, to explore the advantage of using molecular methods to establish the etiology of enteric diseases and to evaluate the prevalence of enteric viruses in asymptomatic human immunodeficiency virus-infected patients. This approach favors rapidity and sensitivity of laboratory diagnosis of viral enteric syndromes.

Adult↗
PubMed2000

Viremia, virus shedding, and antibody response during natural avian polyomavirus infection in parrots.

OBJECTIVE: To determine rapidity of spread and onset and duration of viremia, virus shedding, and antibody production in parrots naturally infected with avian polyomavirus (APV). DESIGN: Case series. ANIMALS: 92 parrots in 2 aviaries. PROCEDURE: Blood samples were obtained from parrots naturally exposed to APV during a 3- to 4-month period for determination of serum virus neutralizing antibody and detection of viral DNA. Nestlings from the next year's hatch were monitored for APV infection. RESULTS: The first indication of inapparent infection was viremia, which developed simultaneously with or was followed within 1 week by cloacal virus shedding and antibody production. Cloacal virus shedding continued after viremia ceased. During viremia, viral DNA was detected continuously in blood samples. Viral DNA was detected in serial cloacal swab specimens in most birds, but it was detected inconsistently in 6 birds and not detected in 3 birds, even though these birds were viremic. Duration of cloacal virus shedding was < or = 4.5 months. In 1 aviary, prevalence of infection was 88% and dissemination of virus through the 3-room building required 4.5 months. In the second aviary, a single-room nursery, prevalence of infection was > or = 90%. For all affected birds, infection could be detected 18 days after the first death. CONCLUSIONS AND CLINICAL RELEVANCE: If a single sampling is used for polymerase chain reaction detection of viral DNA, blood and cloacal swab specimens are required. In nestling nonbudgerigar parrots, cloacal virus shedding may persist for 4.5 months. Management protocols alone are sufficient to prevent introduction of APV into a nursery.

Animals↗
PubMed1984

Some aspects of virus shedding by rainbow trout (Salmo gairdneri Rich.) after waterborne infection with viral haemorrhagic septicaemia (VHS) virus.

VHS virus shedding after experimental waterborne infection of rainbow trout was quantified by measuring virus infectivity in blood, faeces, and urine of catheterised fish. Virus shedding by urine with relatively high yields of infectious virus could be demonstrated during acute VHS until death, but not by faeces. Trout, which were vaccinated against VHS or had survived the disease but showed no detectable humoral antibodies, may excrete infectious virus via urine for more than 30 days and without any signs of VHS after a secondary challenge infection. These results reveal the development of a carrier status of rainbow trout after VHS exposure.

Animals↗
PubMed2000

Comparison of the safety, vaccine virus shedding, and immunogenicity of influenza virus vaccine, trivalent, types A and B, live cold-adapted, administered to human immunodeficiency virus (HIV)-infected and non-HIV-infected adults.

Fifty-seven human immunodeficiency virus (HIV)-infected (CDC class A1-2) and 54 non-HIV-infected adults, not prescreened for influenza susceptibility, were randomized to receive trivalent live attenuated influenza vaccine (LAIV) or placebo intranasally. LAIV was safe and well tolerated with no serious adverse events attributable to vaccine. Reactogenicity rates were similar in LAIV and placebo recipients except that runny nose/nasal congestion was significantly more common in LAIV recipients regardless of HIV status. No prolonged shedding of LAIV was observed in HIV-infected participants. HIV RNA levels were not increased and CD4 counts were not decreased in HIV-infected LAIV recipients compared with placebo recipients after immunization. Shedding of LAIV and increases in antibody titers were infrequent, consistent with prior experience in unscreened adults. The data suggest that inadvertent vaccination with LAIV in relatively asymptomatic HIV-infected adults would not be associated with frequent significant adverse events.

Adult↗
PubMed1975

Hazards from simian herpes viruses: reactivation of skin lesions with virus shedding.

A new simian herpes virus with biological properties similar to herpes simplex and to simian "B" virus has been used as a model system for studying virus latency in dorsal root spinal sensory ganglia. Following intradermal injection, virus is present in the skin lesions and corresponding ganglia only, during the acute stage of the disease. By organ-culture techniques, latent virus was rescued from ganglia up to 2 years later. No latent virus was ever found in skin organ cultures of the primary site. Treatment with cortisone up to 18 months later reactivated virus latent in the ganglia, and virus returned to the skin where it produced small but typical herpes lesions which shed virus. Reactivation of Herpesvirus tamarinus was achieved after 28 months. This is believed to be the first report of a model system for the study of herpes latency in which skin lesions are found to recur, and provides an opportunity for more detailed investigations of the mechanisms of virus latency in man. The presumption that reactivation of skin lesions will also be possible in rhesus monkeys seropositive for "B" virus points to a possibly grave and largely unsuspected hazard for those engaged in primate research.

Animals↗
PubMed1998

Postexposure vaccination with a virion host shutoff defective mutant reduces UV-B radiation-induced ocular herpes simplex virus shedding in mice.

A herpes simplex virus type 1 (HSV-1) recombinant (UL41NHB) deficient in the virion host shutoff (vhs) function was tested as a therapeutic vaccine in an ultraviolet (UV) light-induced mouse ocular reactivation model. Mice were infected with HSV-1 via the cornea. Following the establishment of latency by HSV-1 the mice were subsequently vaccinated intraperitoneally with one dose of UL41NHB or with uninfected cell extract. Mice were subsequently UV-irradiated to induce viral reactivation and during the 7 days post-UV irradiation, numbers of mice shedding virus were reduced from 13/23 (57%) to 3/25 (12%), and numbers of virus-positive eye swabs were reduced from 40/161 (25%) to 6/175 (3%) by the vaccine (P < 0.001). These data suggest that deletion of vhs may be a useful strategy in the development of attenuated therapeutic HSV vaccines.

Animals↗
PubMed2004

Herpes simplex virus type 2 transmission: risk factors and virus shedding.

The prevalence of herpes simplex virus type 2 (HSV-2) infection is not uniform, with some populations bearing a greater burden of disease than others. Potential risk factors that influence HSV-2 transmission rates have been identified, largely from observational prospective and retrospective studies. Risk factors can be categorized as biological or behavioural. These risk factors can be markers of population subgroups that are likely to have acquired, or are at high risk of acquiring, HSV-2. Major factors associated with HSV-2 seropositivity include female gender, race (black), history of sexually transmitted infections, increasing numbers of sexual partners, sexual contact with commercial sex workers and low socio-economic status or level of education. Age-related risk factors are important, likely reflecting the cumulative number of sex partners, age of initiation of sexual activity, and duration of sexual activity as well as chronic nature of HSV-2 infection. Understanding and identifying these factors may help to direct interventions to reduce HSV-2 transmission and acquisition. An important contributing factor to the spread of genital herpes is unrecognized virus shedding, often allowing transmission from individuals who are not aware that they are infected or who are not having a recurrence. Antiviral therapy reduces both the frequency and amount of HSV reactivation, whereas behavioural risk factors can be addressed in part with educational initiatives. Clinical history is a poor predictor of HSV-2 infection and type-specific serological testing is recommended to detect HSV-2 seropositivity.

CD4 Lymphocyte Count↗
PubMed2003

Humoral immune response and assessment of vaccine virus shedding in calves receiving modified live virus vaccines containing bovine herpesvirus-1 and bovine viral diarrhoea virus 1a.

Susceptible calves were administered modified live virus (MLV) vaccines containing bovine herpesvirus-1 (BHV1) and bovine viral diarrhoea type 1 (BVDV1a) strains intramuscularly, with one vaccine containing both MLV and inactivated BHV-1 and inactivated BVDV1a. There was no evidence of transmission of vaccine (BHV-1 and BVDV1a) strains to susceptible non-vaccinated controls commingled with vaccinates. No vaccinates had detectable BHV-1 in peripheral blood leucocytes (PBL) after vaccination. Each of three vaccines containing an MLV BVDV1a strain caused a transient BVDV vaccine induced viremia in PBL after vaccination, which was cleared as the calves developed serum BVDV1 antibodies. The vaccine containing both MLV and inactivated BHV-1 induced serum BHV-1 antibodies more rapid than MLV BHV-1 vaccine. Two doses of MLV BHV-1 (days 0 and 28) in some cases induced serum BHV-1 antibodies to higher levels and greater duration than one dose.

Animals↗
PubMed2003

Comparison of quantitative reverse transcription-PCR to viral culture for assessment of respiratory syncytial virus shedding.

Respiratory syncytial virus (RSV) has recently been recognized as a serious pathogen in elderly and immunocompromised adults. Diagnosis of acute infection in adults is often difficult due to the insensitivity of viral culture, and reverse transcription-PCR (RT-PCR) is a more sensitive alternative. The relationship of quantitative RT-PCR to viable virus has never been studied for RSV. Therefore, we compared a quantitative real-time RT-PCR with viral culture to assess viral load in adult volunteers challenged with the RSV A2 strain. Twelve of 13 volunteers were infected, and there was a high correlation (r = 0.84) between quantitative RT-PCR and viral titer by cell culture. However, RT-PCR was more sensitive, with 73 of 169 (43%) samples positive compared to 58 (34%) samples positive by culture. The correlation between the two tests was highest early in the course of viral shedding (r = 0.91, days 0 to 6), whereas during days 7 to 13, there was more variability (r = 0.70). All subjects were culture negative by day 11, whereas one subject remained RT-PCR positive on day 12. All subjects were RT-PCR negative at day 28 postinfection. Quantitative RT-PCR has an excellent correlation with viral titers, as measured by culture, and should be a useful tool for future studies addressing viral load and disease pathogenesis.

Adult↗
PubMed1978

Virus shedding by SV40-transformed human cells.

Cultures of human cells transformed by SV40 were found to release infectious virus, even after several passages in vitro. Virus shedding by these cultures did not depend on propagation of virus from cell to cell, as it was not affected by anti-SV40 antiserum that could effectively block virus propagation in acutely infected cells. Cells transformed by the 'early' temperature-sensitive mutant tsA30, and maintained at the restrictive temperature of 39 degrees, shed virus in reduced amount. Finally, xeroderma pigmentosum cells transformed by SV40 were also found to release virus, indicating that the enzymes of excision and repair of UV-induced damage to DNA probably were not involved in the molecular mechanism underlying virus shedding.

Antibodies, Viral↗
PubMed2004

The effect of a killed porcine reproductive and respiratory syndrome virus (PRRSV) vaccine treatment on virus shedding in previously PRRSV infected pigs.

Two experiments were conducted to investigate if virus shedding could be reduced following a killed porcine reproductive and respiratory syndrome virus (PRRSV) vaccination (KV) of PRRSV infected pigs. In experiment 1, PRRSV infected pigs were vaccinated with KV on days 14 and 28 following infection. Viremia and serum neutralizing (SN) antibody were compared to infected pigs with no KV. The second experiment was conducted in an identical manner. In addition to viremia and SN antibody, virus in oropharyngeal scrapings and interferon gamma (IFN-gamma) producing cells were monitored. Magnitude and duration of viremia were not different between KV vaccinated and non-vaccinated groups. No virus was detected in oropharyngeal scraping from any pig, nor was there a difference in the detection of viral RNA. In both experiments, however, increases in SN titer and number of IFN-gamma producing cells were observed. The SN titer was significantly higher in KV vaccinated groups than in non-vaccinated group on days 42 and 42-56 following infection in experiments 1 and 2, respectively. The number of IFN-gamma producing cells was slightly higher in KV vaccinated groups than in non-vaccinated group on days 42 and 63. These observations suggest that KV had no effect on virus shedding. However, previously infected pigs responded immunologically to KV, as demonstrated by increases in SN antibody titers and IFN-gamma producing cells.

Animals↗