PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Virus Shedding”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
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↗
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↗
PubMed1975

Increased virus shedding with aspirin treatment of rhinovirus infection.

In two double-blind trials, volunteers challenged with rhinovirus were treated with aspirin or placebo. Aspirin treatment did not alter the rates of infection or illness but was associated with a moderate reduction in the frequency or severity of some symptoms. The overall benefit in rhinovirus infection was not statistically significant. Aspirin treatment appeared to cause a highly significant increase in the rate of virus shedding in treated subjects. The increase in virus shedding must be considered an adverse event that could influence the course of the disease in the individual and increase the likelihood of the spread of the infection to contacts.

Adult↗
PubMed1976

Infectious mononucleosis. Epstein-Barr-virus shedding in saliva and the oropharynx.

In an examination of excretion patterns of Epstein-Barr virus in 104 throat washings from 20 patients with infectious mononucleosis we found that three persons regularly shed virus from the second week through the third month after onset; 15 demonstrated intermittent excretion over three months, and in two cases, no virus was detected. In oral secretions, the virus appeared to be located extracellularly. Transforming activity was demonstrated in aliquots after centrifugation and filtration, in a sample in which cells were disrupted before filtration, and in specimens after two years' storage. Multiple oropharyngeal sites were examined for presence of the virus. In one patient, virus was regularly demonstrated in throat washings and saliva; swabs from Stensen's duct orifices yielded virus in three of four cases. Demonstration of virus in these oropharyngeal specimens explains increased transmissibility in age groups in which salivary exchange is high.

Adolescent↗
PubMed1977

Reliable in vivo model for latent herpes simplex virus reactivation with peripheral virus shedding.

A long-sought laboratory model, a reliable system for in vivo reactivization of latent herpes simplex infection with peripheral shedding of active virus, is present. Results demonstrate that surgical stimulation of latently infected rabbit trigeminal ganglia induces peripheral release of infectious herpes simplex virus. Virus could be cultured from the tear film in 83% of the stimulated animals' eyes within 48 h.

Animals↗
PubMed1977

Quantitative transmissible gastroenteritis virus shedding patterns in lactating sows.

To test the role of sows in spreading transmissible gastroenteritis (TGE), 11 sows were intravenously, intranasally, or intramammarily inoculated with virulent virus within 5 days of farrowing. Six of the sows were separated from their offspring, and 5 were allowed to nurse their litters. All sows became clinically ill with sign of anorexia, depression, and fever that persisted until postinoculation day 4 or 5. They shed virus through milk, nasal secretions, and feces, with individual variations occurring in degree and duration of shedding in the 1st week after inoculation. Of 40 pigs separately fed milk samples from the 6 inoculated sows, 19 pigs (47.5%) became sick in 24 to 40 hours, and virus was isolated from them at necropsy. Of 43 pigs in the 5 litters that nursed exposed dams, all became sick with typical signs of TGE, and 29 (67.4%) died in 2 to 9 days. Sows given the single intramammary inoculation of virus developed statistically significant higher levels of TGE virus-neutralizing antibodies than did sows inoculated intravenously or intranasally.

Administration, Intranasal↗
PubMed1979

Persistence of virus shedding in asymptomatic women after recovery from herpes genitalis.

One hundred seventeen women were reexamined within 6 months after presenting with genital herpes. Swabs for virus isolation were taken from the cervix whether or not lesions were observed. Herpesvirus type II was isolated from 30 of 67 patients with recurrent disease, but also from 5 of 50 women during periods when there were no signs or symptoms of illness. The epidemiologic importance of virus shedding from asymptomatic women is discussed.

Adult↗
PubMedDate not supplied

Live attenuated influenza vaccines in young seronegative children.

Seronegative children undergoing primary infection sensitively reflect the residual virulence of an experimental attenuated respiratory vitral vaccine. Two temperature sensitive (ts) A/Hong Kong influenza vaccines derived following chemical mutagenesis of a cloned stock of A/Great Lakes/65 have been evaluated in vaccine trials in seronegative children. The two vaccines, ts-1[A] and ts 1[E], differ in their laboratory characteristics. Ts-1[A] has a lower shut-off temperature, 37 degrees C vs 38 degrees C, and more limited replication in the Syrian hamster model system than ts-1[E]. In A/HK seronegative adults ts-1[A] is noninfectious whereas ts-1[E] will replicate and induce an antibody response. The genetic lesion of ts-1[A] was stable in the young child; in contrast, late in the course of virus shedding, ts-1[E] exhibited genetic instability with 4 individuals shedding virus which had lost the ts marker. Transmission to controls was rare with both vaccines being observed in only 1 of 5 controls with ts-1[A] and none of six controls with ts-1[E]. There were no respiratory symptoms associated with ts-1[A] vaccine virus shedding. Ts-1[E] virus shedding had a suggestive association with fever and cough in the seronegative child. The trials in seronegative children extent and confirm the inherent differences between ts-1[A] and ts-1[E] vaccine strains and support the concept that laboratory markers of attenuation are predictive of vaccine behavior in the seronegative child.

Administration, Intranasal↗
PubMed1979

Viral shedding patterns of children with influenza B infection.

During an epidemic of influenza B, 43 ambulatory children were prospectively followed to determine the quantitative shedding patterns of influenza B viral infection, because these have not been previously described. The spectrum of illness included 74% with a typical influenzalike illness, 7% with an afebrile infection of the upper respiratory tract, and 19% with croup. Mild myositis occurred in 21%. For the first three days of illness, greater than or equal to 93% of the children shed virus, and 74% shed on day 4. The average peak quantity of virus shed in the nasal wash was 4.0 log10 50% tissue culture infective doses/ml(range, 1.5-6.0), which gradually declined over four days to 2.4 log10 50% tissue culture infective doses/ml. The quantities of virus shed correlated significantly with severity of illness and fever score, but not with sex, type of illness, or occurrence of myositis. These results suggest that the degree of clinical illness may be directly related to the cytotoxic effects of the virus and to the transmissibility of the disease.

Adolescent↗
PubMed1975

Transmission of cytomegalovirus infection with renal allograft.

Fifty-four patients who received a renal allograft between October 1971 and October 1974 were followed prospectively to correlate pretransplant serum antibody to cytomegalovirus (CMV) with shedding of CMV following transplantation. Twenty-five of 54 patients had antibody demonstrable to CMV using immunofluorescent techniques, but only 20 of 54 using complement-fixing techniques. All 24 who had antibody and survived one month or longer, and seven of nine without antibody but who received a kidney from a seropositive donor shed virus after transplantation, whereas none of 12 individuals without antibody and who received a kidney from a seronegative donor (P less than 0.005) shed virus. Three of eight other seronegative patients for whom donor sera were not available for analysis shed virus. Viremia occurred in eight of ten individuals who developed new antibody after transplantation, versus seven of 24 with antibody prior to transplant (P less than 0.02), and virus shedding in seroconverters from other sites was significantly more persistent than in pretransplant antibody-positive patients. Thus, CMV infection was due either to reactivation of latent infection or was transmitted along with the renal allograft and manifested as a primary infection.

Adult↗
PubMed1975

Cervical cytomegalovirus excretion in pregnant and nonpregnant women: suppression in early gestation.

Comparison of 659 pregnant and 202 nonpregnant women with similar demographic characteristics showed overall rates of cervical cytomegalovirus excretion that were identical (9.5% vs. 9.4%) and were surprisingly high, especially since 89% of the pregnant group possessed antibody to cytomegalovirus when admitted to the study. Prevalence of cytomegalovirus among gravidas was significantly lower during the first (1.6%) than during the third (11.3%) trimester. Thus, early pregnancy appeared to exert a suppressive effect on viral excretion that waned with advancing gestation. A similar but less significant occurrence was observed in the two groups with respect to viuria. Increasing age also appeared to suppress the virologic expression of cervical and urinary tract infection, whereas multiparity seemingly produced such an effect only in the cervix. Among both cervical and urinary excreters, a few shed virus thoughout pregnancy, and others shed virus intermittently; however, viral shedding most commonly began in late gestation and frequently continued into the postpartum period. Primary infection was not documented, and antibody status remained unchanged with the advent of viral excretion in most cases. Thus, reactivation of endogenous virus seems the most likely explanation for viral shedding in our population. Similar rates of isolation of Neisseria gonorrhoeae in excreters and nonexcreters further argue against the other major possibility, venereal reinfection.

Amniotic Fluid↗
PubMedDate not supplied

Duck plague: a carrier state in waterfowl.

Healthy waterfowl were found to be carriers of duck plague (DP) virus. Black ducks (Anas rubripes) and Canada geese (Branta canadensis) surviving a natural outbreak of DP at Coloma, Wisconsin, in 1973 yielded DP virus in cloacal swabs taken four years postinfection. Experimental infection of previously unexposed mallard ducks (Anas platyrhynochos) with the Coloma strain of DP virus CO-WI (73) also produced cloacal virus shedding for up to four years after infection. A second DP virus strain, LA-SD (73) from the Lake Andes, South Dakota, epornitic, was detected from cloacal swabs of pintail ducks (Anas acuta), gadwall ducks (Anas strepera), wood ducks (Aix sponsa), and Canada geese infected experimentally one year before. The frequency of swabs positive for DP virus varied between individuals within each of the tested species. The amount of detectable DP virus shed was about 100 plaqueforming units of virus percloacal swab. Oral erosions were present in all species tested except Canada geese and gadwall ducks. Erosions occurred at the openings of the sublingual salivary gland ducts. DP virus was isolated from erosions. All ducks with lesions proved to shed DP virus, although not necessarily at the time they had the lesion.

Animals↗
PubMed1978

Evaluation of five temperature-sensitive mutants of respiratory syncytial virus in primates: II. Genetic analysis of virus recovered during infection.

Five temperature-sensitive (ts) mutants of respiratory syncytial (RS) virus (ts-1, ts-1 NG-1, ts-1 NG-16, ts-2, and ts-7), previously evaluated forinfectivity and virulence in chimpanzees and owl monkeys, were also assayed for in vivo genetic stability. None of the five mutants tested was completely stable genetically. Thus, virus which had lost some or all of the ts property was recovered from each infected chimpanzee. Significantly, each ts-1 NG-1 isolate retained some degree of temperature sensitivity and hence was not true wild-type virus. Clonal analysis of viruses shed by ts-1, ts-1 NG-1, ts-1 NG-16, or ts-7 infected chimpanzees indicated that in most instances only a minority of the virus shed was altered genetically. Of five chimpanzees infected with the ts-2 mutant, three shed only ts virus, and the remaining two chimpanzees shed only ts+ virus. Such ts+ virus proved to be avirulent when evaluated in chimpanzees or owl monkeys, indicating that loss of the ts property did not restore virulence. Based upon these findings, the ts-2 mutant appears to be a suitable candidate for clinical trials in man.

Animals↗