Showing papers on "Viremia published in 1985"

Experimental infection with Puumala virus, the etiologic agent of nephropathia epidemica, in bank voles (Clethrionomys glareolus).

Abstract: Subclinical chronic infections characterized by transient viremia, prolonged virus shedding in oropharyngeal secretions and feces, and virus persistence in tissues (particularly lung) developed in laboratory-bred weanling bank voles (Clethrionomys glareolus) inoculated intramuscularly with Puumala virus (strain Hallnas), the etiologic agent of nephropathia epidemica. Viral antigen, as evidence by granular fluorescence, was detected in the lungs, liver, spleen, pancreas, salivary glands, and small intestine. Infectious virus was found in the lungs from 14 to 270 days postinoculation, and feces and urine collected 35 to 130 days postinoculation were regularly and sporadically infectious, respectively. Horizontal transmission coincided with virus shedding in oropharyngeal secretions. Suckling voles also developed asymptomatic persistent infections after intracerebral inoculation, and histopathological changes were absent despite widespread infection. Our data resemble findings in Apodemus agrarius experimentally infected with Hantaan virus, the prototype virus of hemorrhagic fever with renal syndrome, suggesting that the mechanisms of maintenance and transmission of Puumala and Hantaan viruses are similar in their respective wild-rodent hosts.

Infection by the Retrovirus Associated with the Acquired Immunodeficiency Syndrome: Clinical, Biological, and Molecular Features

Abstract: Peripheral mononuclear cells from more than 160 persons from groups at risk for the acquired immunodeficiency syndrome (AIDS) have yielded AIDS-associated retroviruses (ARV). Antibodies to ARV can also be found in these risk groups. Antibody-negative, virus-positive persons have been identified with early infection or possible viremia with immune complex formation. Established lines of human T and B cells, monocytes, and promyelocytes have been infected with ARV. Moreover, infectious virus has been recovered from macrophages cultured from the blood of some persons with AIDS. The cytopathic effects of ARV in T cells is associated with the accumulation of unintegrated viral forms in the infected cells. The ARV has also been isolated from plasma, serum, saliva, semen, urine, cerebrospinal fluid, and brain tissue. All these results reflect the wide host range of ARV and support its role in neurologic abnormalities seen in some patients. Molecular studies of independent ARV isolates indicate a polymorphism of nucleotide sequences, particularly in the viral envelope region. All these features place ARV in the lentivirus subfamily of human retroviruses.

Viral replication and immunologic responses in children naturally infected with varicella-zoster virus and in varicella vaccine recipients.

Abstract: Replication of varicella-zoster virus (VZV) and immunologic responses to VZV were examined by a sensitive culture technique for viral isolation and standard immunologic assays in children after close exposure to wild-type VZV or after inoculation with strain Oka varicella vaccine. Naturally infected children who developed clinical varicella had viremia between five days before and one day after clinical onset of disease, with the highest isolation rate one and two days before onset, and seroconversion followed two days later. Virus was not isolated from blood 12 and 13 days after contact in subclinically infected children. In the vaccine recipients a positive skin test reaction to VZV was observed as early as four to five days after immunization, and antibody appeared later. Virus was not isolated from blood and throat of the vaccinees from three to 14 days after immunization.

Pathogenesis of Canine Parvovirus Enteritis: Sequential Virus Distribution and Passive Immunization Studies

Abstract: After oral inoculation, the sequential distribution of canine parvovirus was studied in 14 nine-week-old seronegative beagle dogs. Two or three dogs were necropsied on days 1 through 6 after inoculation. Tissues were collected for virus isolation, immunofluorescence testing, and light microscopy. Virus was isolated from, and fluorescent cells were seen in the tonsil, retropharyngeal and mesenteric lymph nodes one and two days after inoculation. Virus infection of systemic and intestinal lymphoid tissues occurred as early as three days after inoculation and was associated with viremia. Intestinal epithelial infection was first seen four days after oral inoculation. All dogs were viremic before intestinal epithelial infection was found. Fecal virus excretion first occurred four days after oral virus inoculation. Intestinal virus infection and lesions became progressively more severe between four and six days after inoculation. The severity of intestinal lesions was variable and related to the severity of systemic lymphoid tissue lesions and the magnitude and duration of viremia. Four littermates of virus-infected dogs were passively immunized against canine parvovirus with convalescent canine serum 24 hours after oral virus inoculation. Neither clinical signs, lymphopenia, nor fecal virus excretion occurred in passively immunized dogs. Intestinal epithelial infection was not demonstrable by immunofluorescence testing when passively immunized dogs were necropsied four, five, and six days after virus inoculation.

Pathogenesis of Hantaan virus infection in suckling mice: clinical, virologic, and serologic observations.

Abstract: Hemorrhagic fever with renal syndrome (HFRS) is a debilitating disease of humans caused by Hantaan virus (HV), the prototype member of a newly proposed genus of Bunyaviridae. Studies of HV pathogenesis have been limited by the absence of a well defined model for a virus-induced disease state. In an attempt to devise a model for HV pathogenesis in laboratory rodents, newborn outbred suckling ICR mice were shown to be uniformly susceptible to lethal infection with non-mouse adapted HV by intracerebral (IC), intraperitoneal (IP), intramuscular (IM), and subcutaneous (SC) inoculation routes. Clinical course, mean time to death, and fatal outcome were age-dependent. With an inoculum of 10 LD50, mortality was 100% in mice infected within 72 hr of birth, but declined to 50% by 7 days. By 2-2.5 weeks, animals developed complete resistance to clinical disease. Virus was consistently detected in serum by day 6 post-infection in IC- and IP-inoculated animals, and reached peak levels of congruent to 10(5) PFU/ml by day 8. Mice infected IM and SC showed delays in onset of viremia, but achieved similar titers. Immunofluorescent antibody appeared by 17-18 days, and neutralizing antibody by 15 days, in all experimental groups. Two of 8 inbred mouse strains were identified as resistant to clinical disease: SJL/J and A/J.

Pathogenesis of Canine Parvovirus Enteritis: The Importance of Viremia

Abstract: The clinical signs, hematologic changes, serum and fecal virus titers, specific antibody production and the occurrence of histologic lesions were studied in 22 nine-week-old seronegative beagle dogs inoculated by the oral and intravenous route with canine parvovirus. Approximately 30% of the dogs had clinical signs of pyrexia, depression, vomiting, and diarrhea irrespective of the route of inoculation. Events in the dogs inoculated intravenously preceded those in dogs inoculated orally by approximately two days. Only one dog died. Lymphopenia was the most consistent hematologic change. Viremia always preceded the initiation of fecal virus shedding. Viral titers in the serum and feces were significantly greater in symptomatic dogs compared to asymptomatic dogs. Termination of the plasma viremia coincided with the onset of the humoral immune response, but viremia persisted one day longer in symptomatic dogs. The severity of lymphoid tissue and intestinal infection, assessed by tissue immunofluorescence and histology, was also greater in symptomatic dogs. The severity of intestinal disease was highly correlated with the magnitude and duration of viremia.

Varicella-Zoster Virus Infection of Strain 2 Guinea Pigs

Abstract: Weanling strain 2 guinea pigs are susceptible to infection with varicella-zoster virus cultured in embryonic guinea pig tissue. Animals inoculated by an intramuscular route develop mononuclear cell viremia that may persist for as long as three weeks. During the period of viremia, virus may be recovered from the nasopharynx and a variety of tissues. In addition, virus may be recovered from neural tissues in the absence of viremia, although infectious virus has not been cultivated from neural tissues after the 23rd day. The strain 2 guinea pig should provide an animal model to study the pathophysiology of infections caused by varicella-zoster virus.

Monoclonal antibodies specific for wild mouse neurotropic retrovirus: detection of comparable levels of virus replication in mouse strains susceptible and resistant to paralytic disease.

Abstract: We used AKR/J mice to produce monoclonal antibodies specific for a neurotropic ecotropic (WM-E) virus initially isolated from wild mice. The rationale for this approach involved the observation that these mice were immunologically hyporesponsive to endogenous ecotropic virus (Akv) but fully responsive to type-specific determinants of WM-E. Hybridoma cell lines derived from mice immunized with both denatured and viable virus produced antibodies with specificity for three viral membrane-associated polypeptides, gp70, p15(E), and p15gag. Epitopes specific for WM-E virus were detected in each of these polypeptides. Cross-reactivity with Friend ecotropic virus (Friend murine leukemia virus) was observed with some gp70- and p15gag-specific antibodies, but no reactivity with endogenous Akv ecotropic virus was seen. The majority of these antibodies did not react with either xenotropic or mink cell focus-forming viruses. Two WM-E-specific anti-gp70 antibodies reacting with different determinants had virus-neutralizing activity in the absence of complement, suggesting that the respective epitopes may participate in receptor binding or virus penetration events. We used these monoclonal antibodies in initial studies to examine the replication of WM-E virus in neonatally inoculated AKR/J mice which are fully resistant to the paralytic disease induced by this virus. Since these mice express high levels of endogenous ecotropic virus, standard assays for ecotropic virus cannot be used to study this question. We present evidence that the resistance to disease does not involve a resistance to virus replication, since these mice expressed levels of viremia and virus replication in spleen and lumbar spinal cord comparable to susceptible NFS/N mice at a time when the latter began to manifest clinical signs of lower-motor-neuron pathology.

Clinical significance of cytomegalovirus viremia in bone marrow transplantation.

Abstract: Cytomegalovirus (CMV) viremia was systematically studied in 56 patients having undergone bone marrow transplantation for leukemia or aplastic anemia. Of the patients who survived at least three months, 57% had CMV viremia with a frequency peak between the 7th and the 9th weeks. We describe possible clinical signs associated with viremia, particularly late peripheral and/or central thrombocytopenia. The occurrence of viremia was studied according to the specific preexisting immune status of recipients and donors; granulocyte transfusions and graft-versus-host disease. The relationship between these parameters and viremia provides a basis for the analysis of prophylactic treatments of CMV infection.

Temporal replication of the Pullman strain of Aleutian disease virus in royal pastel mink.

Abstract: Information was sought on the temporal replication of Aleutian disease virus in 27 royal pastel mink. Groups of three were examined 8 to 126 days after they were inoculated subcutaneously with 10(3) 50% lethal doses of the Pullman strain. Much individual variation was noted in the onset of infection, occurrence of viremia, and extent of virus replication in the tissues. Thus, virus was detected in lymph nodes regional to the site of inoculation in only some mink during the first 14 days after inoculation. During this period, virus was often present as well in the mesenteric lymph node and spleen. First detected on day 10, viremia was present in all mink examined on day 28 but occurred irregularly thereafter, even when virus was widespread in the tissues. Except in five mink succumbing to the disease, the tissue distribution of virus after day 28 tended to be more limited, and the titers were generally lower than they had been earlier. Even though present in the lymph nodes and spleen, virus was often absent from the kidney, liver, and intestine after day 28. Specific antibody was detected on day 28 and was present in all mink thereafter, ostensibly without any adverse effect on virus replication. In most mink, the infection was considered subclinical, for it was usually not accompanied by a rise in serum gamma globulin or by morphologic evidence of the disease. The virologic findings in this study have a bearing on the relationship of subclinical infections to both horizontal and vertical transmission of the virus.

Equine herpesvirus type 2: cell-virus relationship during persistent cell-associated viremia.

Abstract: Some aspects of the biology of equine herpesvirus type 2 (EHV-2) were investigated by examination of the persistent cell-associated viremia stage of the infection. The EHV-2 infection of leukocytes was latent, because free virus was not retrieved without first cultivating harvested leukocytes in vitro. A virus infective center (IC) assay was developed to enumerate latently infected cells in the leukocyte population. This assay proved to be simple and reproducible and revealed a linear relationship between IC plaques formed and the number of cells inoculated, except where large numbers of cells (greater than 4 X 10(6)) were inoculated per 10 cm2 dish. This reduction at high cell densities of IC/10(6) cells inoculated was dependent on cells obtained from an EHV-2-infected horse. There was considerable variation in the numbers of IC/10(6) leukocytes harvested from different horses, but little variation in the harvests from the same horse at different times. There seemed to be a direct relationship between serum-neutralization titers and IC numbers. Transfer of viable infected leukocytes to 2 fetuses failed to establish EHV-2 infection. Infection of equine fetal kidney cells with EHV-2 virus failed to produce detectable Fc receptors on the cell surface.

La Crosse Viremias in Juvenile, Subadult and Adult Chipmunks (Tamias striatus) Following Feeding by Transovarially-Infected Aedes Triseriatus*

Abstract: Viremia and antibody responses to La Crosse (LAC) virus were determined for juvenile, subadult and adult chipmunks (Tamias striatus). Viremia was detected in 16 of 16 juveniles, 13 of 17 subadults and 21 of 29 adults fed upon by transovarially (TO)-infected Aedes triseriatus. Mean viremia titers for juvenile, subadult and adult chipmunks responding to LAC infection were 3.0, 2.9 and 3.2 log10SMICLD50/0.025 ml, respectively. The average duration of viremia with LAC virus was 2.4, 2.3 and 2.4 days for juveniles, subadults and adults, respectively. Mean viremia titers and durations did not differ significantly among chipmunk age-classes. Neutralizing antibodies to LAC virus were detected in viremic chipmunks at day 5 and day 20 post-infection. Observations of TO-infected Ae. triseriatus and their sibling controls refeeding on restrained chipmunks indicated that a significant number of infected (34/54) and uninfected (37/59) females probed multiple times to obtain a second bloodmeal. Data indicate that chronological age or time between successive bloodmeals affects feeding behaviors. No relationship between probing or ability to refeed and infection was found.

Isolation of bluetongue virus from bull semen.

Abstract: The efficacy of inoculation of Vero cell cultures or intravenous inoculation of chicken embryos in the isolation and titration of seminal bluetongue virus (BTV) was studied, as was the toxicity of bull semen for these 2 isolation systems. Frozen and thawed BTV-contaminated ejaculates collected during periods of viremia from 2 bulls experimentally infected with cell culture-adapted BTV serotype 17 were used in isolation, titration and fractionation studies. Blood collected from the 2 bulls concurrently with the semen was titrated in chicken embryos. Bull semen was toxic for both isolation systems. Toxicity was associated with both the spermatozoa and seminal plasma. Dilution of the semen at least 1:25, addition of peptone or tryptose broth to the diluent, limitation of adsorption time and postinoculation washing of cell culture monolayers all reduced the destructive effects of semen. Isolation of BTV was successful from 11 ejaculates and was titratable in 9 of these. Blind passage of surviving embryos or cell cultures at the endpoints of the titrations produced BTV isolations in 4 instances. The virus was never isolated from semen in the absence of concurrent viremia. Peak seminal BTV titers of 10(5.5) CEIVLD50/ml and 10(5.7) TCID50/ml were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of Antibody Infusion on Pathogenesis of Experimental Feline Leukemia Virus Infection

Abstract: For examination of the influence of antibody on the pathogenesis of feline leukemia virus (FeLV) infection, 12 weanling specific-pathogen-free cats were inoculated with isolates of FeLV and were treated beginning at 7, 19, 21, 24, 34, or 49 days post inoculation (DPI) with feline anti-FeLV hyperimmune serum (10 infusions, 37 mg globulin/kg each at 48-hr intervals). Anti-FeLV serum infusion initiated at 7 DPI prevented the onset of hematopoietic cell infection and viremia. Antibody treatment initiated at 19 or 24 DPI abrogated recently established FeLV viremia and extinguished p27 expression in bone marrow and blood cells. Viremia established for longer periods was refractory to antibody infusion despite establishment of enzyme-linked immunosorbent assay antibody titers of 1:80 to 1:320 in the treated cats. Latent FeLV infection was a sequel to antibody-induced curtailment of viral replication in bone marrow cells and was able to reactivate spontaneously in vivo as well as in vitro.

An overview of Colorado tick fever.

Abstract: Certain features of Colorado tick fever (CTF) virus and the disease it causes may be relevant to studies on bluetongue virus (BTV), or other orbiviruses. Rapid and easy detection of viral antigen in infected tissues and peripheral blood cells by immunofluorescence staining facilitate diagnosis of the disease. The prolonged (3-4 months) viremia is due to persistent intracellular infection, particularly of erythrocytes, in which the virus is protected from antibody or other host defense mechanisms. This results in more efficient maintenance of the virus cycle in nature, but might lead to adverse effects in the human host. Clues to understanding chronic viral infections or viral immunosuppression might be gained by further research on CTF and other orbiviruses.

Oral infection and transmission of La Crosse virus by an enzootic strain of Aedes triseriatus feeding on chipmunks with a range of viremia levels.

Abstract: The susceptibility of Aedes triseriatus to oral infection with La Crosse (LAC) virus resulting from feeding on chipmunks with viremia titers of 0.6 to 4.6 log10SMICLD50/0.025 ml was determined. Results indicated that viremia titers must exceed 3.2 log10SMICLD50/0.025 ml before a significant proportion (greater than or equal to 50%) of mosquitoes are infected and capable of transmitting LAC virus. Mosquitoes which fed on chipmunk blood-LAC virus mixtures through a membrane feeder had significantly lower infection rates at virus titers of 1.8 to 4.4 log10SMICLD50/0.025 ml and transmission was also significantly reduced. Application of these data to LAC viremia titers measured in chipmunks in an earlier study indicate that viremias sufficiently high to ensure transmission by the mosquitoes becoming orally infected average only about 1 day per infective bite delivered to the susceptible portion of the amplifier population. Oral infection and transmission rates were also determined for Ae. triseriatus feeding on chipmunk blood containing LAC virus neutralizing (N) antibodies and for Ae. triseriatus feeding on deer blood containing Jamestown Canyon (JC) virus N antibodies. Infection rates were similar to those observed in mosquitoes imbibing blood free of N antibody at the virus titers tested, but, oral transmission was reduced in females feeding on chipmunk blood-LAC virus mixtures containing LAC N antibodies and there was no transmission by females feeding on deer blood-LAC virus mixtures containing JC N antibodies. These data suggest that high LAC antibody prevalences in chipmunk populations and high LAC or JC antibody prevalences in deer populations may be antagonistic to horizontal LAC virus transmission.

Spontaneous expression of C-type virus in DBA/2 mice is associated with an increased rate of mortality, independent of neoplastic disease.

Abstract: Ecotropic C-type retroviruses isolated from both normal and dimethylbenzanthracene-treated DBA/2 mice could be classified into three major groups, Ea, Eb, and Ec, that differed in structure and biology. Weanling DBA/2 mice were generally free of viruses, but a fraction of adult individuals became virus positive and were apparently selectively associated with a high expression of the Eb viruses. Some of the ecotropic viruses from DBA/2 mice acted as exogenous pathogens. They caused viremia and a moderate incidence of leukemia when injected into C3H and ST/a mice. In addition, they caused an appreciable number of early deaths without signs of malignancy. To evaluate the natural role of the viruses, we studied the survival of spontaneously viremic and nonviremic DBA/2 mice. The viremic animals as a group were characterized by a significantly reduced life-span that was not related to neoplasia. These observations indicated that endogenous C-type retroviruses can be pathogenic without preselection of the host for disease. They also emphasize that endogenous viruses, like their exogenous counterparts, can have a broader pathogenic spectrum than normally appreciated.

Pathogenesis of attenuated Junin virus in the guinea pig model.

Abstract: The purpose of this work was to elucidate the pathogenesis of attenuated Junin virus (JV) strains in the guinea pig model. Three groups of guinea pigs were infected by the IM route with 103 PFU of the XJC13 and XJO-attenuated strains or with the XJ pathogenic strain of JV, respectively. Viremia was studied at 3, 5, 7, 9, 12, and 14 days postinfection (pi) (a) in serum samples of all animals and in washed cells from XJC13-infected guinea pigs by conventional techniques and (b) in whole blood samples from XJC13 and XJO animals by coculture with Vero cells. Virus spread was studied at 14 days pi in brain, spleen, lymph nodes, and bone marrow by parallel suckling mouse inoculation or organ homogenates and coculture of cell suspensions with Vero cells. By coculture techniques of whole blood, an otherwise undetectable viremia was demonstrated for both attenuated strains throughout the observation period. In contrast, XT viremia was easily detected by direct techniques, as has already been shown. Attenuated virus was also shown to reach brain and bone marrow when coculture methods were employed. But titers were always markedly lower than those of the pathogenic strain. The sustained viremia demonstrated in guinea pigs infected with either attenuated strain explains the mode of viral dissemination and accounts for viral rescue and antigen detection from some organs. These results suggest that attenuated strains do not differ greatly in their invasive capacity in guinea pigs, but later on viral replication is impaired. Therefore, these findings reveal potential risks and should be noted when developing human vaccines.

Isolation of Junin virus from blood and peripheral lymphocytes of infected Calomys musculinus

Abstract: Neonatal Calomys musculinus experimental infection with Junin virus (JV) XJCl3 strain causes either death or a persistent infection in the major part of surviving animals. JV can be isolated from peritoneal macrophages early during infection, and from brain and salivary glands during the chronic state of disease. It was of interest to investigate the appearance of virus in blood of infected animals. For this purpose, we decided to study the development of viremia in inoculated cricetids. A high frequency of viremia was registered during the acute state of disease (figure 1), which became sporadic approximately from 20 days post-infection onwards. Considering the results above mentioned, the characteristic lymphotropism of arenaviruses and the well-known JV replication in human mononuclear cells, cultures of lympho-monocytes obtained from blood of infected C. musculinus were done in order to investigate the eventual detection of infectious virus in the supernatants. JV was isolated, although in low titres, from cultures established with mononuclear cells belonging to animals in the acute state of disease (table 1); in the case of chronically infected cricetids, attempts to isolate JV were negative. These results show that viremia is currently detected in experimentally infected C. musculinus and that circulating mononuclear cells are permissive for JV multiplication, during the acute state of disease.

Prevention of Transmission of Virus Infections by Blood Transfusions and Removal of Virus Infectivity from Clotting Factor Concentrates

Abstract: Virus infections are serious complications following blood transfusions or intravenous therapy with clotting factor concentrates. Hepatitis A virus (HAV) is rarely transmitted by blood and never by plasma derivatives. Hepatitis A is characterized by a short viremia which most often coincides with clinical illness. In addition neutralizing antibodies to HAV are present in all plasma pools from which clotting factor concentrates are manufactured (1). Chronic Hepatitis B and non-A non-B hepatitis commonly follow acute infections (5 to 10% for hepatitis B, more than 40% and perhaps close to 100% for non-A non-B hepatitis). Chronic infections with hepatitis B virus (HBV) are characterized by serum levels of infectious virus up to 108/ml (infectious units) while levels of infectious non-A non-B virus are generally in the range of 102/ml (2,3). Little has been published concerning levels of HTLV III in blood or plasma.

Humoral and cellular immune response of sheep to bluetongue virus.

Abstract: Plaque cloned strains of the 4 US bluetongue (BT) virus (BTV) serotypes (10, 11, 13 and 17) were pathogenic to sheep and induced mild clinical responses. The clinical responses coincided with the highest titer of viremia reached by day 7 following primary infection. The 4 BTV strains were immunogenic, inducing group-specific (precipitating) and type-specific (neutralizing) antibodies. Primary infection induced an immune response which protected the animals against secondary challenge with the homologous virus. Peripheral blood lymphocytes (PBL) obtained from infected animals responded specifically to in vitro stimulation with pure BT viral antigens. PBL responded to both homologous and heterologous BTV antigens indicating a cross-reactive nature of the lymphocyte response. Perturbations were observed in PBL response to in vitro stimulation with the mitogens phytohemagglutinin (PHA), concanavalin A (Con A), and pokeweed mitogen (PWM). The response to mitogens was depressed transiently following primary infection and secondary challenge. A significant increase was reached by 3 weeks following primary infection and then gradually leveled off to normal. The specific stimulation of PBL in response to viral antigens and the increase in response to mitogens, as in vitro correlates of cell mediated immunity (CMI), were suggested to play a role in the clearance of BTV infection. Immunoblotting was applied to characterize the specificity of the serologic response to BTV. Sheep antisera to BTV detected 11 specific viral proteins. The maximum response on day 28 post inoculation (PI) detected 11 proteins including both the major and minor protein components.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies on pathogenesis of buffalo pox virus in rabbits: quantitative assay of virus in different organs.

Abstract: The buffalo pox virus was found to multiply in the skin, the primary site of inoculation with an eclipse phase of 12 hr. The virus was then detected in the skin after 15 hr followed by its appearance in regional lymph nodes 36 hr postinoculation. Primary viremia was detected 48 hr postinoculation, followed by detection of virus in the lungs, liver, and spleen. The virus multiplied in the lungs on day 4 and in the liver and spleen on day 5 postinoculation and its release led to secondary viremia. In a follow-up from day 7 to 14 postinoculation, the virus was detected in the kidneys, stomach, intestines, and gonads.

Experimental Studies of the Pathogenesis of Feline Leukemia Virus Infection

Abstract: Feline leukemia virus (FeLV) infection is transmissible by contact exposure, by oral-nasal or parenteral inoculation, and by congenital exposure of outbred cats to FeLV. The susceptibility vs resistance of cats to FeLV is determined by early containment vs amplification of retroviral replication in target hemolymphatic cells. The course of these pivotal early events is age-dependent, macrophage-dependent, and corticosteroid-sensitive. Either of two host-virus relationships ensue in cats exposed to FeLV: (a) progressive infection characterized by persistent viral replication in hemolymphatic and epithelial cells, persistent viremia, minimal anti-viral immune response, and a high risk of subsequent disease, or (b) regressive infection characterized by transient retroviral replication in hemolymphatic cells, abrogation of viremia, and a low incidence of subsequent disease. Some regressively infected cats harbor persistent latent FeLV infection in certain hemolymphatic cells. Such residual non-productive FeLV infections may be reactivated, transmitted congenitally, or be involved in the genesis of virus-negative leukemias. Although less notorious than leukemogenesis, it is the cytosuppressive disease syndromes which constitute the predominant pathogenic manifestations of FeLV infection in cats.

Incidence and Significance of Cytomegalovirus Viremia in Bone Marrow Transplantation

Abstract: In immunosuppressed patients (pts), cytomegalovirus (CMV) viremia is an accurate marker for disseminated CMV infection as opposed to urine excretion or changes in antibody titers. A systematic study of CMV viremia was serially performed after allogenic transplantation (BMT) in 96 pts whose the clinical manifestations related to viremia were described. The occurrence of viremia was examined according to graft versus host disease (GVHD) and pts or donor pretransplant immunity against CMV.

Approach to the Patient with Aseptic Meningitis or Encephalitis

Abstract: Numerous viral infections can affect the central nervous system (CNS), causing a spectrum of disease entities. Viruses shown to cause CNS infections are both RNA and DNA viruses that infect the patient, multiply in specific organs, and then are transferred into the CNS secondary to a viremia.