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Biomedical subjects

N C Pedersen

Publications and source records attributed to N C Pedersen.

At least 127 records · Page 7Linked to original sources
PubMed1989

Epidemiologic and clinical aspects of feline immunodeficiency virus infection in cats from the continental United States and Canada and possible mode of transmission.

The epidemiologic features of feline immunodeficiency virus (FIV) infection were evaluated in 2,765 cats from the United States and Canada. Of these cats, 2,254 were considered by veterinarians to be at high risk for the infection, and 511 were healthy cats considered to be at low or unknown risk. Of the cats in the high-risk group, 318 (14%) were found to be infected with FIV. The infection rate among low- or unknown-risk cats was 6 of 511 (1.2%). Male cats in the high-risk group were 3 times more likely to be infected than were females, similarly as were cats greater than 6 years old, compared with younger cats; domestic cats, compared with purebred cats; and free-roaming cats, compared with confined cats. Feline immunodeficiency virus and FeLV infections did not appear to be linked with each other; 16% of FeLV-infected cats in the high- and low-risk groups were coinfected with FIV. In contrast, there was a pronounced linkage between FIV and feline syncytium-forming virus (FeSFV) infections. Seventy-four percent of FeSFV-infected cats in the high-risk study group were coinfected with FIV, compared with a 38% FIV infection rate among cats that were not infected with FeSFV. The major clinical manifestations associated with FIV infection in cats that were surveyed included chronic oral cavity infections (56%), chronic upper respiratory tract disease (34%), chronic enteritis (19%), and chronic conjunctivitis (11%). Bacterial infections of the urinary tract (cystitis), skin, and ears were seen in a small proportion of cats.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1989

Feline immunodeficiency virus infection in cats of Japan.

A seroepidemiologic survey for feline immunodeficiency virus (FIV) infection was conducted in Japan. Between June and December 1987, individual sera (n = 3,323) were submitted by veterinary practitioners from many parts of the country. Specimens were from 1,739 cats with clinical signs suggestive of FIV infection and from 1,584 healthy-appearing cats seen by the same practitioners. The overall FIV infection rate among cats in Japan was 960/3,323 cats (28.9%). The infection rate was more than 3 times higher in the clinically ill cats, compared with that in the healthy cats of the same cohort (43.9 vs 12.4%). Male cats were 1.5 times as likely to be infected as were females. Almost all FIV-infected cats were domestic cats (as opposed to purebred cats). Complete clinical history was available for 700 of 960 FIV-infected cats. Of these 700 FIV-infected cats, 626 (89.4%) were clinically ill, and the remainder did not have clinical signs of disease. The mean age at the time of FIV diagnosis for the 700 cats was 5.2 years, with younger mean age for males (4.9 years) than for females (5.8 years). Most of the infected cats (94.7%) were either allowed to run outdoors or had lived outdoors before being brought into homes. The mortality for FIV-infected cats during the 6 months after diagnosis was 14.7%, and the mean age at the time of death was 5.7 years. Concurrent FeLV infection was seen in 12.4% of the FIV-infected cats, but this was not much different from the historical incidence of FeLV infection in similar groups of cats not infected with FIV.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1989

Feline immunodeficiency virus infection.

Feline immunodeficiency virus (FIV) (formerly feline T-lymphotropic lentivirus or FTLV) was first isolated from a group of cats in Petaluma, California in 1986. The virus is a typical lentivirus in gross and structural morphology. It replicates preferentially but not exclusively in feline T-lymphoblastoid cells, where it causes a characteristic cytopathic effect. The major structural proteins are 10, 17 (small gag), 28 (major core), 31 (endonuclease?), 41 (transmembrane?), 52 (core precursor polyprotein), 54/62 (reverse transcriptase?), and 110/130 (major envelope) kilodaltons in size. The various proteins are antigenically distinguishable from those of other lentiviruses, although serum from EIAV-infected horses will cross-react with some FIV antigens. Kittens experimentally infected with FIV manifest a transient (several days to 2 weeks) fever and neutropenia beginning 4 to 8 weeks after inoculation. This is associated with a generalized lymphadenopathy that persists for up to 9 months. Most cats recover from this initial phase of the disease and become lifelong carriers of the virus. Complete recovery does not occur to any extent in nature or in the laboratory setting. One experimentally infected cat died from a myeloproliferative disorder several months after infection. The terminal AIDS-like phase of the illness has been seen mainly in naturally infected cats. It appears a year or more following the initial infection in an unknown proportion of infected animals. FIV has been identified in cats from all parts of the world. It is most prevalent in high density populations of free roaming cats (feral and pet), and is very uncommon in closed purebred catteries. Male cats are twice as likely to become infected as females. Older male cats adopted as feral or stray animals are at the highest risk of infection, therefore. The infection rate among freely roaming cats rises throughout life, and reaches levels ranging from less than 1% to 12% or more depending on the area. Clinically affected cats tend to be 5 years or older at the time of hospitalization. Experimental and seroepidemiologic studies suggest that FIV is transmitted mainly by bites. Intimate, non-traumatic contact (mutual grooming, shared use of food, water and litter pans) is inefficient in transmitting the infection. In utero and venereal transmission could not be demonstrated in laboratory settings. There is no statistical linkage between FIV and feline leukemia virus (FeLV) infections in nature. The FeLV infection rate in FIV-infected animals is the same as it is for non-FIV-infected cats.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1989

Nucleotide sequence and genomic organization of feline immunodeficiency virus.

An infectious molecular clone of the Petaluma strain of feline immunodeficiency virus (FIV) was isolated from a recombinant bacteriophage library containing genomic DNA prepared from FIV-infected Crandall feline kidney (CRFK) cells. The integrated provirus has a total length of 9472 base pairs. Three long open reading frames corresponding to GAG, POL, and ENV gene coding frames are evident. In addition, an open reading frame overlaps the 3' end of POL, in the region that encodes viral infectivity factor in the primate viruses. Several short open reading frames are present in the intergenic region between POL and ENV and within ENV, which may serve as exons for production of TAT and REV equivalents in FIV. Alignment of the predicted amino acid sequences of the FIV proteins with those of other lentiviruses indicates that FIV did not arise recently from any other characterized lentivirus.

Amino Acid Sequence↗
PubMed1989

Cyclosporine pharmacokinetics in cats following topical ocular administration.

Topical ocular administration of two forms of cyclosporine were studied in the cat. Both forms were able to produce measurable whole-blood levels capable of suppressing in vitro lymphocyte stimulation. The kinetics of cyclosporine following administration of either oral solution or cyclosporine in olive oil were variable, with peak concentrations ranging from 450 to 1033 ng/ml and 288 to 648 ng/ml, respectively. Absorption lag time ranged from 0 to 1.34 hr for oral solution, and 0.27 to 1.2 hr for cyclosporine in olive oil. The half-life of elimination ranged from 2.41 to 10.04 hr, and 3.09 to 15.75 hr, respectively. When compared with the commercially available oral solution, cyclosporine dissolved in olive oil was better tolerated during administration. Topical ocular administration of cyclosporine in cats offers a possible alternative method of treatment for individuals intolerant of oral administration. Topical ocular administration might also replace the need for intravenous administration of cyclosporine during perioperative periods or during periods of vomiting and nausea associated with rejection or other illnesses. Due to individual variation in absorption and elimination of topically applied cyclosporine, dosages in each cat must be determined by monitoring blood, plasma, or serum levels.

Administration, Topical↗
PubMed1989

Feline immunodeficiency virus, a model for reverse transcriptase-targeted chemotherapy for acquired immune deficiency syndrome.

Feline immunodeficiency virus (FIV), formerly called feline T-lymphotropic lentivirus, causes an immune deficiency in cats that is very similar to the acquired immune deficiency syndrome in humans (N. C. Pedersen, E. M. Ho, M. L. Brown, and J. K. Yamamoto, Science 235:790-793, 1987). We have examined the reverse transcriptase of this virus to determine whether it is similar enough to the reverse transcriptase of the human immunodeficiency virus type 1 (HIV-1) to enable its use as a model for chemotherapy for acquired immune deficiency syndrome. The FIV reverse transcriptase is similar to that of HIV-1 in sensitivity to the noncompetitive inhibitor phosphonoformate (Ki, 0.3 microM) and relative insensitivity to phosphonoacetate. This enzyme was also sensitive to two competitive inhibitors, the 5'-triphosphates of 2', 3'-dideoxythymidine (Ki, 3.4 nM) and 3'-azido-3'-deoxythymidine (AZT; Ki, 6.2 nM). The ratios of Ki/Km for these two competitive inhibitors are similar to the ratios calculated from previously reported data for the HIV-1 enzyme assayed under identical conditions. In contrast, the FIV enzyme is different from the reverse transcriptase of avian myeloblastosis virus in sensitivity to those inhibitors. The replication of FIV in Crandell feline kidney cells was inhibited by AZT; virus production was inhibited more than 95% by 1.0 microM AZT.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Development and evaluation of immunoassay for detection of antibodies to the feline T-lymphotropic lentivirus (feline immunodeficiency virus).

The feline T-cell lymphotropic lentivirus (feline immunodeficiency virus) is a recently described feline-specific retrovirus that can produce chronic immunodeficiency-like disorders in cats. A microdilution plate format enzyme-linked immunosorbent assay has been developed to detect the presence of antibody to the virus in feline serum or plasma. Temporal studies performed with experimentally infected animals show that seroconversion can be demonstrated 3 to 4 weeks after exposure to the virus. Results of a serosurvey (n = 1,556 samples) indicate that infection is fairly common in both clinic (5.2%) and sick cat (15.2%) populations. Western blot (immunoblot) and sodium dodecyl sulfate radioimmunoprecipitation assays were developed to confirm microdilution plate test results and to identify peptides specific for the feline immunodeficiency virus. All microdilution plate test positive results and selected negative results were confirmed by one or both of these procedures. These data demonstrate that this microassay plate enzyme-linked immunosorbent assay is a very sensitive and specific test for detection of antibody to the feline immunodeficiency virus.

Animals↗
PubMed1989

Infection of peritoneal macrophages in vitro and in vivo with feline immunodeficiency virus.

Macrophages were harvested from the peritoneal cavities of healthy specific-pathogen-free cats by saline lavage. Three days before collection, the peritoneal cavities were stimulated with glutaraldehyde-fixed Saccharomyces cerevisiae cells to induce greater numbers of macrophages and to begin the activation sequence. Peritoneal macrophages from cats stimulated once with yeast consisted mainly of small macrophages and a smaller number of larger activated macrophages. After several days in culture, many of the small macrophages became activated and a portion of the activated macrophages developed into multinucleated giant cells. Peritoneal cells from cats that were stimulated twice or three times with yeast at 3-week intervals consisted of a higher proportion of activated macrophages initially and produced more and larger multinuclear giant cells with time. Cultures of peritoneal cells stimulated once with yeast were easily infected in vitro with feline immunodeficiency virus (FIV) and produced a transient burst of reverse transcriptase activity. After the initial burst of virus replication, the infection became latent. Even more multinucleated giant cells appeared after infection, and many of these cells fused with each other. Replicating virus could be rescued from the latently infected macrophages after 2 to 3 weeks of phorbol myristate acetate stimulation and cocultivation with T-lymphocyte-enriched peripheral blood mononuclear cells. Multiply stimulated peritoneal cells, which contained a much higher proportion of activated macrophages, could also be infected in vitro with FIV. The infection usually became latent, however, without going through an initial replicative stage. Peritoneal cells from chronically FIV-infected specific-pathogen-free cats contained a higher proportion of activated macrophages and were latently infected with FIV from the outset.

Animals↗
PubMed1989

Rhesus macaques inoculated with molecularly cloned simian immunodeficiency virus.

We have isolated a biologically active molecular clone of simian immunodeficiency virus (SIV), SIVmac 1A11, originally obtained from a rhesus macaque at the New England Regional Primate Research Center. Virus derived from cells transfected with this clone is cytopathic for rhesus peripheral blood mononuclear cells, replicates in cultures of rhesus macrophages, and infects rhesus macaques when inoculated intravenously. Six macaques inoculated with SIVmac 1A11 all became infected and produced antibodies to viral envelope glycoproteins that neutralized virus. Antibodies to viral core proteins were detected in only one animal. No clinical signs of disease were observed throughout 7 months postinoculation.

Animals↗
PubMed1989

[Cat retroviruses and human retroviruses: elements of comparison].

Following emotional head-lines of certain articles in the press, making believe that the cat could be susceptible to the AIDS virus, the authors present elements of comparison between principal feline retroviruses (the feline leucosis virus and the feline immunodeficiency virus) and the two human immunodeficiency viruses (HIV). The feline leucosis virus in differentiated from the human and the feline immunodeficiency viruses by its virological, pathological and epidemiological characteristics. Being close to the AIDS virus in the taxonomy of retroviruses, the feline immunodeficiency virus (FIV) presents a number of similarities with the HIV. Therefore, the FIV could give rise to interests in its use as a model in the study of AIDS. Whatever the factors of resemblances may be, there are no elements of present knowledge in favor of an inter-species contamination (cat-man); on the contrary, these viruses demonstrate a marked species specificity.

Acquired Immunodeficiency Syndrome↗
PubMed1988

The detection of conventional class I and class II I-E homologue major histocompatibility complex molecules on feline cells.

The presence on feline cells of class I and class II I-E type major histocompatibility complex (MHC) homologues was demonstrated using cross-reacting monoclonal antibodies (mAb). The feline class I antigen homologues were detected with both immunofluorescent and biochemical techniques, using the anti-human class I mAb W6/32. The class I antigens were detected on in vitro cultured feline fibroblasts and lymphoid cells, but not on fresh lymphoid cells, apparently as a result of the association of bovine beta-2 microglobulin with feline class I heavy chains which generated the determinant(s) recognized by mAb W6/32. Class II I-E-like molecules could be detected with immunofluorescent techniques using the species cross-reactive anti-mouse I-E antibody 40D only when peripheral blood mononuclear cells were activated, for example, with the mitogens staphylococcus enterotoxin A or lipopolysaccharide. The predominant expression of I-A-like molecules by resting class II-positive feline cells could explain some of the functional difference we have seen in comparison with those of most other mammalian species.

Animals↗
PubMed1988

Simian retrovirus-D serotype 1 (SRV-1) envelope glycoproteins gp70 and gp20: expression in yeast cells and identification of specific antibodies in sera from monkeys that recovered from SRV-1 infection.

The gp70 and transmembrane gp20 envelope proteins of simian retrovirus-D serotype 1 (SRV-1) were expressed in Saccharomyces cerevisiae as fusion proteins with human superoxide dismutase (SOD). Expression of the SOD-gp70 and SOD-gp20 sequences yielded fusion proteins of 52 and 29 kilodaltons, respectively. The yeast-expressed SRV-1 envelope proteins were used in an enzyme-linked immunosorbent assay (ELISA) for the detection of antibodies in the sera of rhesus macaques that recovered from SRV-1. Sera from 47 of 49 such monkeys tested positive for antibodies to the SOD-gp70 fusion protein, while 45 of 49 reacted positively to SOD-gp20. None of 26 SRV-1-nonexposed monkeys tested positive in either ELISA. Monkeys immunized with the recombinant SRV-1 gp20 and gp70 proteins made good ELISA and Western blot (immunoblot) antibodies to whole SRV-1. This antibody was not neutralizing in vitro, however.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Pathogenesis of experimentally induced feline immunodeficiency virus infection in cats.

Feline immunodeficiency virus (FIV; formerly, feline T-lymphotropic lentivirus) is a typical lentivirus resembling human and simian immunodeficiency viruses in morphologic features, protein structure, and reverse transcriptase enzyme. It is antigenically dissimilar, however. The virus is tropic for primary and permanent feline T-lymphoblastoid cells and Crandell feline kidney cells. The virus did not grow in other permanent feline non-lymphoblastoid cells that were tested, or in lymphoid and non-lymphoid cells from man, dogs, mice, and sheep. During short-term inoculation studies in cats, the feline immunodeficiency-like syndrome found in nature was not experimentally induced, but a distinct primary phase of infection was observed. Fever and neutropenia were observed 4 to 5 weeks after inoculation; fever lasted several days, and neutropenia persisted from 1 to 9 weeks. Generalized lymphadenopathy that persisted for 2 to 9 months appeared at the same time. Antibodies to FIV appeared 2 weeks after inoculation and then plateaued. Virus was reisolated from the blood of all infected cats within 4 to 5 weeks after inoculation and persisted indefinitely in the face of humoral antibody response. Virus was recovered from blood, plasma, CSF and saliva, but not from colostrum or milk. Contact transmission was achieved slowly in one colony of naturally infected cats, but not between experimentally infected and susceptible specific-pathogen-free cats kept together for periods as long as 4 to 14 months. The infection was transmitted readily, however, by parenteral inoculation with blood, plasma, or infective cell culture fluids. In utero and lactogenic transmission were not observed in kittens born to naturally or experimentally infected queens. Lymphadenopathy observed during the initial stage of FIV infection was ascribed to lymphoid hyperplasia and follicular dysplasia. A myeloproliferative disorder was observed in 1 cat with experimentally induced infection.

Animals↗
PubMed1988

Feline immunodeficiency syndrome--a comparison between feline T-lymphotropic lentivirus and feline leukemia virus.

A feline T-lymphotrophic lentvirus (FTLV) has recently been isolated from a domestic cat free of feline leukemia virus (FeLV). This virus is distinct from FeLV (an oncornavirus), although they share a common denominator, namely, the ability to cause immunosuppression and induce lymphadenopathy and anemia. Their differences can be revealed by examining the following: the metal requirement for reverse transcriptase activity, the antigenic comparison by Western blot analysis, the different susceptibilities of a variety of feline cells, and the morphology based on electron microscopy. In the serological survey of 1,612 cats surveyed in the USA, 232 (14.4%) were seropositive for antibodies to FTLV, which was lower than for the 42 Canadian cats surveyed of which 8 (19%) were seropositive. Of the 61 cats positive for FeLV, 15 (25%) were also positive for FTLV, giving the impression that coinfection between these two retroviruses plays an important role in the cliniocpathological signs of what was previously thought to be solely an FeLV syndrome.

Animals↗
PubMed1987

Isolation of a T-lymphotropic virus from domestic cats with an immunodeficiency-like syndrome.

A highly T-lymphotropic virus was isolated from cats in a cattery in which all the animals were seronegative for feline leukemia virus. A number of cats in one pen had died and several had an immunodeficiency-like syndrome. Only 1 of 18 normal cats in the cattery showed serologic evidence of infection with this new virus, whereas 10 of 25 cats with signs of ill health were seropositive for the virus. Tentatively designated feline T-lymphotropic lentivirus, this new feline retrovirus appears to be antigenically distinct from human immunodeficiency virus. There is no evidence for cat-to-human transmission of the agent. Kittens experimentally infected by way of blood or plasma from naturally infected animals developed generalized lymphadenopathy several weeks later, became transiently febrile and leukopenic, and continued to show a generalized lymphadenopathy 5 months after infection.

Animals↗
PubMed1987

Virologic and immunologic aspects of feline infectious peritonitis virus infection.

A number of feline coronavirus isolates have been characterized over the last few years. These isolates consist of what we have referred to as feline enteric coronaviruses (FECVs) and feline infectious peritonitis viruses (FIPVs). FECVs cause a transient enteritis in kittens but no systemic illness. FIPVs, in contrast, cause a systemic and usually fatal disease syndrome characterized either by an exudative serositis or a disseminated granulomatous disease. Although the diseases they cause are quite different, FECVs and FIPVs are antigenically and morphologically indistinguishable from each other. FECVs have a strict tropism for mature intestinal epithelial cells and do not appear to replicate in macrophages. In contrast, FIPVs, appear to spread rapidly from the intestinal mucosa and replicate in macrophages. Experiments will be presented, and literature cited, that will allow us to make the following assumptions about the pathogenesis of FIPV infection: 1) FIPVs and FECVs represent a spectrum of viruses that differ only in infectivity (ability to evoke seroconversion following oral infection) and virulence (ability to cause FIP), 2) field isolates are generally nearer to FECVs in behavior than laboratory isolates made from animal passaged material, 3) immunity to FIPV appears to be of the premunition type and is maintained for as long as the infection persists in a reactivatable form, 4) strains of feline coronaviruses that do not cause systemic disease, such as FECVs or low virulence FIPVs, can actually sensitize cats to infection with virulent FIPV strains, 5) FeLV infection interferes with established FIP immunity and allows for the reactivation of disease in healthy carriers, 6) FIPV may be passaged from queen to kitten either in utero or during neonatal life, and 7) kittens infected by their mothers with FIPV do not usually develop FIP but become immune carriers of the virus for a period of 5-6 months; recovery from the carrier state is associated with a loss of premunition immunity.

Animals↗