Search PubMed⌕ Search

Biomedical subjects

N C Pedersen

Publications and source records attributed to N C Pedersen.

At least 55 records · Page 3Linked to original sources
PubMed1998

Bartonella henselae antibody prevalence in free-ranging and captive wild felids from California.

In order to determine the importance of wild felids in the epidemiology of Bartonella spp. infection, 136 Nobuto strips or serum samples from free-ranging mountain lions (Felis concolor) and bobcats (Felis rufus) captured in California (USA) between 1985 and 1996 were tested for B. henselae antibodies (titer > or = 1:64) using an immunofluorescence test. Similarly, 124 serum samples from 114 captive wild cats representing 26 species or subspecies collected between 1991 and 1995 were retrieved from the serum banks of four California zoological parks. Fifty-three percent (33/62) of the bobcats, 35% (26/74) of the mountain lions, and 30% (34/114) of the captive wild felids (genera Acinonyx, Panthera and Felis) had B. henselae antibodies. In captive wild felids, prevalence varied widely among the species, but seropositivity was more likely to occur in the genus Felis than in the genus Acinonyx or Panthera. Prevalence was evenly distributed between sexes, except for free-ranging mountain lions. Antibody prevalence ranged from 25% in 0- to 2-yr-old captive felids to 35% in cats > or = 9-yr-old, but the highest antibody titers were observed in cats < 5-yr-old.

Age Factors↗
PubMed1998

Molecular, clinical, and pathologic comparison of two distinct strains of Haemobartonella felis in domestic cats.

OBJECTIVE: To characterize 2 strains of Haemobartonella felis by use of molecular techniques. ANIMALS: 35 specific-pathogen-free cats, 6 months to 4 years old. PROCEDURE: Intraperitoneal or IV inoculation with blood containing H felis small form (Hfsm, 18 cats) or H felis large form (Hflg, 11 cats); 6 cats were uninfected controls. Hfsm was evaluated for capability to cross-protect against the more virulent Hflg. Morphology of both strains was compared by light microscopy of Wright-Giemsa-stained blood smears, and the 16S rRNA genes were sequenced. RESULTS: Infection with Hflg induced signs of depression, fever, and severe macrocytic normochromic anemia with nucleated erythrocytes. More than 95% of erythrocytes were parasitized. Inoculation with Hfsm and uninfected control blood induced mild or no clinical signs and no hematologic abnormalities. Anti-H felis IgG was first detected on postinoculation day (PID) 21, and increased to maximal titer of 400 by PID 28. Reactivated infection was observed in 8 of 29 cats (4 Hfsm and 4 Hflg), with 5% parasitized erythrocytes during the later attack. On PID 8, Hflg-inoculated cats had positive results of polymerase chain reaction analysis (PCR) that persisted until cats were treated with doxycycline or oxytetracycline; Hfsm-inoculated cats had positive PCR results that persisted for duration of observation (3 months). CONCLUSIONS: Genetically and morphologically distinct strains of H felis infect cats in the field. The level of genetic difference suggested that these strains may be different species or genera. CLINICAL RELEVANCE: PCR is a critical diagnostic aid to detect occult Haemobartonella spp infection, as well as response to treatment and clearance of the organism.

Anaplasmataceae↗
PubMed1997

Patterns of feline coronavirus infection and fecal shedding from cats in multiple-cat environments.

OBJECTIVE: To determine, by use of a reverse transcriptase-polymerase chain reaction (RT-PCR) test, patterns of fecal shedding of feline coronavirus among cats. DESIGN: Prospective observational study. ANIMALS: 275 purebred cats from 6 private catteries and 40 specific-pathogen-free (SPF) laboratory-reared cats. PROCEDURE: 40 SPF cats were experimentally inoculated with crude fecal extract containing feline enteric coronavirus (FECV). Fecal and plasma samples were collected every 4 days and evaluated by use of RT-PCR and indirect immunofluorescence assays, respectively, to correlate RT-PCR results with fecal infectivity and to determine patterns of FECV shedding and anti-FECV IgG production in acutely infected cats. The 275 cats in private catteries were monitored for 1 year. Fecal and blood samples were collected every 1 to 3 months and assayed by use of RT-PCR and serologic tests to determine patterns of coronavirus shedding and cofactors for high frequency shedding. RESULTS: Results of the RT-PCR test in SPF cats were directly correlated with fecal extract infectivity. Overall, 370 of 894 (41%) fecal samples collected from cattery and shelter cats contained infectious levels of coronavirus. Of 121 cats from which multiple samples were collected, 11 never shed virus and 35, 65, and 10, respectively, shed virus with low, moderate, and high frequency. High frequency shedding was associated with age and cattery of origin, but not with sex or concurrent disease. Stress associated with parturition and lactation did not induce shedding in queens. Kittens did not shed coronavirus before they were 10 weeks old, even when nursed by shedding mothers. CLINICAL IMPLICATIONS: A large proportion of cats in multiple-cat environments shed coronavirus at any given time, but most undergo cycles of infection and shedding, recovery, and reinfection. Infection is acquired from chronically shedding cats and from infectious cats undergoing transient primary infection. Chronically shedding cats cannot be identified on the basis of antibody titer or signalment, but must be identified on the basis of the results of serial fecal RT-PCR tests.

Animals↗
PubMed1997

Risk factors for feline infectious peritonitis among cats in multiple-cat environments with endemic feline enteric coronavirus.

OBJECTIVE: To determine what risk factors, other than genetic predisposition, contribute to the incidence of feline infectious peritonitis (FIP) in private breeding catteries and animal shelters. DESIGN: Cats from 7 catteries and a shelter were observed monthly for 1 year. At each visit, cats were examined, fecal samples were collected for determination of feline coronavirus shedding, and blood samples were collected for determination of coronavirus antibody titers. Diagnostic tests were performed on all cats that died of FIP. ANIMALS: 275 purebred or random-bred cats that were kept by private breeder-owners in homes. RESULTS: 24 cats died of FIP during the study. Development of FIP was not associated with cattery, mean cat number, mean age, sex, cattery median coronavirus antibody titer, husbandry and quarantine practices, caging and breeding practices, or prevalence of concurrent diseases. However, risk factors for FIP included individual cat age individual cat coronavirus titer, overall frequency of fecal coronarvirus shedding, and the proportion of cats in the cattery that were chronic coronavirus shedders. Deaths from FIP were more frequent in fall and winter, and on the basis of analysis of cattery records, the number of deaths varied yearly. Epidemics (> 10% mortality rate) were reported at least once in 5 years in 4 catteries. CLINICAL IMPLICATIONS: Elimination of FIP from a cattery is only possible by total elimination of endemic feline enteric coronavirus (FECV) infection. The most important procedure to reduce FECV from catteries is elimination of chronic FECV shedders.

Age Factors↗
PubMed1997

Experimental and natural infection with Bartonella henselae in domestic cats.

Domestic cats were experimentally infected with culture propagated Bartonella henselae by intradermal (i.d.) and intravenous (i.v.) routes. Cats were more efficiently infected by the i.d. (8/8 cats) than by the i.v. (2/16) route. Bacteremia was detected 1-3 weeks following inoculation and lasted for most cats for 1-8 months. However, one naturally infected cat was observed for 24 months and was found to be cyclically bacteremic, with bacterial levels varying one hundred fold or more from one period to another. No clinical or hematologic abnormalities were observed in any of the infected cats, even at the peak of bacteremia. Two cats that had become abacteremic were resistant to reinfection when inoculated with B. henselae a second time. Horizontal transmission through intimate contact between bacteremic and susceptible cats did not occur, and antibody positive bacteremic queens did not transmit the infection to their kittens in utero, peri-partum or post-partum. Only four of the 18 kittens acquired detectable levels of maternal antibody following nursing, which disappeared by 6 weeks of age. These studies indicate that B. henselae exists in an almost perfect host-parasite relationship with its feline host, but that most cats can ultimately rid themselves of the infection. The susceptibility of cats to intradermal infection and the lack of direct cat-cat transmission are compatible with possible arthropod vectors.

Animals↗
PubMed1997

Toxicity associated with high dosage 9-[(2R,5R-2,5-dihydro-5-phosphonomethoxy)-2-furanyl]adenine therapy off attempts to abort early FIV infection.

9-[(2R,5R-2,5-dihydro-5-phosphonomethoxy)-2-furanyl]adenine, or D4API, was tested in the feline immunodeficiency virus (FIV) infection model and found to be significantly more inhibitory in vitro than its parent compound 9-phosphonylmethoxethyl adenine (PMEA). Cytotoxicity was less than for PMEA or azidothymidine (AZT) for culture periods of 7 days, but more toxic after 10 days. D4API was rapidly absorbed by cats following subcutaneous inoculation, with a plasma half-life of less than 1 h after intravenous inoculation and between 2 and 3 h after subcutaneous injection. Peripheral blood mononuclear cells collected from cats given a single dose of D4API were refractory, however, to FIV infection in vitro for up to 24 h. Given its prolonged intracellular phase and high selectivity index, high dose D4API therapy was tested for its ability to abort an acute (i.e. 2 week) FIV infection. A divided daily dose of D4API, which was one-fourth the toxic dose and 125 times the concentration that would totally inhibit virus replication in vitro, completely abrogated the anticipated viremia and antibody responses. Unfortunately, a majority of treated/uninfected and treated/infected test cats died acutely of drug toxicity after 47 days of treatment. Toxicity in vivo mirrored what was observed in vitro, being precipitous and cumulative in nature. Toxic signs included widespread hepatic and lymphoid necrosis. A surviving treated/FIV infected cat remained healthy to day 175 when the study was terminated; antibodies appeared 2 months later than in untreated/infected cats and virus was only detectable at low levels on day 175. In contrast, untreated/infected cats were viremic and antibody positive from 3 to 4 weeks post-infection onwards. Therefore, it was possible to alter, but not abort, an early FIV infection with prolonged, high-dose D4API treatment.

Adenine↗
PubMed1997

A zidovudine-resistant simian immunodeficiency virus mutant with a Q151M mutation in reverse transcriptase causes AIDS in newborn macaques.

The simian immunodeficiency virus (SIV)-newborn rhesus macaque model of AIDS can be used to study directly the virulence of viral mutants which are resistant to antiviral drugs. A viral mutant called SIVmac79A6.1, isolated from an SIV-infected macaque after prolonged zidovudine treatment, was found to have a double-base-pair change at codon 151 of reverse transcriptase, resulting in a glutamine to methionine substitution (Q151M). This mutation was associated with more than 100-fold increased resistance to zidovudine and low-level cross-resistance to other dideoxynucleoside analogs. To determine whether this Q151M mutation affects viral virulence, four newborn macaques were inoculated intravenously with a biological clone of this drug-resistant SIVmac79A6.1 mutant; two of these animals were also treated orally with zidovudine. All four animals showed persistent viremia, and two of the four animals developed fatal immunodeficiency at 3 and 8 months of age, respectively. The remaining two animals had CD4+ T-cell depletion and clinical symptoms of AIDS at 22 months. No phenotypic or genotypic reversion of virus to the wild type could be detected in any of the four animals. These results demonstrate that the Q151M mutation in SIV reverse transcriptase does not reduce viral virulence.

Animals↗
PubMed1997

Immunopathologic changes in the thymus during the acute stage of experimentally induced feline immunodeficiency virus infection in juvenile cats.

The feline thymus is a target organ and site of viral replication during the acute stage of feline immunodeficiency virus (FIV) infection. This was demonstrated by histologic, immunohistologic, flow cytometric, and virologic tests. Thymic lesions developed after 28 days postinoculation (p.i.) and included thymitis, premature cortical involution, and medullary B-cell hyperplasia with germinal center formation and epithelial distortion. Alterations in thymocyte subsets also developed. Fewer CD4+ CD8- cells were detected at 28 days p.i., while an increase in CD4- CD8+ cells resulted in an inversion of the thymic CD4/CD8 ratio of single-positive cells, similar to events in peripheral blood. Provirus was present in all thymocyte subpopulations including cortical CD1(hi), CD1(lo), and B cells. The CD1(hi) thymocyte proviral burden increased markedly after 56 days p.i., coincident with the presence of infiltrating inflammatory cells. Increased levels of provirus in the CD1(lo) thymocyte subpopulation were detected prior to 56 days p.i. This was likely due to inclusion of infected infiltrating inflammatory cells which could not be differentiated from mature, medullary thymocytes. Proviral levels in B cells also increased from 70 days p.i. Morphologic alterations, productive viral infection, and altered thymocyte subpopulations suggest that thymic function is compromised, thus contributing to the inability of FIV-infected cats to replenish the peripheral T-cell pool.

Acute Disease↗
PubMed1997

Nucleotide and predicted peptide sequence of feline interleukin-12 (IL-12).

Feline Interleukin-12 (IL-12) is a heterodimeric glycoprotein consisting of two disulfide linked subunits of about 40 kD (p40) and 35 kD (p35). It is a pleiotropic cytokine mediating biological activities on T- and NK-cells. One important function is the induction of a Th1 immune response. Here we report the cloning and sequencing of feline IL-12, the expression of the p40-protein in E. coli and production of monoclonal antibodies. At the nucleotide level, feline IL-12 shows between 87-90%, on the amino acid level between 82-87% identity to the bovine and human IL-12, respectively.

Amino Acid Sequence↗
PubMed1996

9-[2-(Phosphonomethoxy)propyl]adenine therapy of established simian immunodeficiency virus infection in infant rhesus macaques.

The long-term therapeutic and toxic effects of 9-[2-(phosphonomethoxy)propyl]adenine (PMPA) were evaluated in simian immunodeficiency virus (SIV)-infected newborn rhesus macaques. Four untreated SIV-infected newborn macaques developed persistently high levels of viremia, and three of the four animals had rapidly fatal disease within 3 months. In contrast, long-term PMPA treatment of four newborn macaques starting 3 weeks after virus inoculation resulted in a rapid, pronounced, and persistent reduction of viremia in three of the four animals. Emergence of virus with fivefold-decreased susceptibility to PMPA occurred in all four PMPA-treated animals and was associated with the development of a lysine-to-arginine substitution at amino acid 65 (K65R mutation) and additional mutations in the reverse transcriptase; however, the clinical implications of this low-level drug resistance are nuclear. No toxic side effects have been seen, and all PMPA-treated animals have remained disease-free for more than 13 months. Our data suggest that PMPA holds much promise for the treatment of human immunodeficiency virus-infected human infants and adults.

Adenine↗
PubMed1996

Two related strains of feline infectious peritonitis virus isolated from immunocompromised cats infected with a feline enteric coronavirus.

Two groups of cats were experimentally infected orally with the cat-passaged RM strain of feline enteric coronavirus (FECV-RM). One group of cats (n = 19) had been chronically infected with feline immunodeficiency virus (FIV) for over 6 years, while a second control group (n = 20) consisted of FIV-naive siblings. Fecal virus shedding of FECV occurred in both groups starting on day 3 postinfection, nearly ceased by 4 weeks in FIV-uninfected cats, but remained at high levels in FIV-infected animals. FIV-infected cats shed virus for a longer period of time and at levels 10 to 100 times greater than those for FIV-uninfected cats. The coronavirus antibody response of the FIV-infected cats was delayed and of reduced titer compared with that of the FIV-uninfected animals. Cats in both groups remained asymptomatic for the first two months following FECV-RM infection; however, 8 to 10 weeks postinfection two cats in the FIV-infected group developed feline infectious peritonitis (FIP). The FIP viruses (designated FIPV-UCD9 and -UCD10) isolated from these two cats had almost complete genetic homology to each other and to the infecting FECV-RM. However, unlike FECV-RM, they readily induced FIP when inoculated intraperitoneally into specific-pathogen-free cats. This study confirms that FIPVs are frequently and rapidly arising mutants of FECV. Immunosuppression caused by chronic FIV infection may have enhanced the creation and selection of FIPV mutants by increasing the rate of FECV replication in the bowel and inhibiting the host's ability to combat the mutant viruses once they occurred.

Animals↗
PubMed1996

Experimental transmission of Bartonella henselae by the cat flea.

Bartonella henselae is an emerging bacterial pathogen, causing cat scratch disease and bacillary angiomatosis. Cats bacteremic with B. henselae constitute a large reservoir from which humans become infected. Prevention of human infection depends on elucidation of the natural history and means of feline infection. We studied 47 cattery cats in a private home for 12 months to determine the longitudinal prevalence of B. henselae bacteremia, the prevalence of B. henselae in the fleas infesting these cats, and whether B. henselae is transmitted experimentally to cats via fleas. Vector-mediated transmission of B.henselae isolates was evaluated by removing fleas from the naturally bacteremic, flea-infested cattery cats and transferring these fleas to specific-pathogen-free (SPF) kittens housed in a controlled, arthropod-free University Animal Facility. B. henselae bacteremia was detected in 89% of the 47 naturally infected cattery cats. A total of 132 fleas were removed from cats whose blood was simultaneously cultured during different seasons and were tested individually for the presence of B. henselae DNA by PCR. B. henselae DNA was detected in 34% of 132 fleas, with seasonal variation, but without an association between the presence or the level of bacteremia in the corresponding cat. Cat fleas removed from bacteremic cattery cats transmitted B. henselae to five SPF kittens in two separate experiments; however, control SPF kittens housed with highly bacteremic kittens in the absence of fleas did not become infected. These data demonstrate that the cat flea readily transmits B. henselae to cats. Control of feline infestation with this arthropod vector may provide an important strategy for the prevention of infection of both humans and cats.

Adult↗
PubMed1996

Proviral burden and infection kinetics of feline immunodeficiency virus in lymphocyte subsets of blood and lymph node.

Feline immunodeficiency virus (FIV) is similar to human immunodeficiency virus type 1 virologically and induces a clinical syndrome in cats comparable to human immunodeficiency virus type 1 syndrome in humans. To determine the lymphoid target cells of FIV, populations of CD4+ lymphocytes, CD8+ lymphocytes, and CD21+ lymphocytes (B cells) were enriched to more than 96.5% purity and then analyzed for FIV provirus by semiquantitative DNA amplification. We found FIV provirus in CD4+, CD8+, and B lymphocytes. In cats infected for <4 months, proviral burden was greatest in CD4+ cells, followed by B cells and then by CD8+ cells. In cats infected for more than 5 years, proviral burden was greatest in B cells, followed by CD4+ cells and then by CD8+ cells. The total proviral burden was > 1 log10 higher in acutely infected cats than in chronically infected cats, primarily because of a higher level of CD4+ infection in the acutely infected cats. A comparison of proviral loads in mesenteric lymph node and peripheral blood mononuclear cells in acutely or chronically infected cats revealed no significant difference. A kinetics study of FIV infection demonstrated that all lymphocyte subpopulations were infected by 4 weeks postinoculation. Virus was isolated from CD4+, CD8+, and B cells in vitro, and reverse transcriptase PCR demonstrated that all subsets contained viral RNA in vivo and therefore are productive reservoirs for FIV.

Animals↗
PubMed1996

Simian immunodeficiency virus infection of CD8+ lymphocytes in vivo.

To determine the lymphoid target cells of simian immunodeficiency virus (SIV) in vivo, peripheral blood lymphocytes (PBL) and lymph node lymphocytes (LNL) were positively selected (>97% purity) for surface expression of CD4, CD8, or CD20 and then analyzed for SIV provirus using semiquantitative DNA amplification. We found provirus in CD4+ and CD8+ lymphocytes but none in CD20+ lymphocytes. During acute SIV infection (< or = 214 days postinoculation), the percentage of PBL and LNL CD4+ cells containing proviral DNA ranged from 0.2 to 20% and from 0.2 to 2%, respectively. Proviral burden in the CD8+ population of either PBL or LNL ranged from 0.01 to 0.2%. Virus isolation by cocultivation was positive for both CD4+ and CD8+ purified populations. No difference in proviral burden was observed between PBL and LNL subsets during acute SIV infection. Up to 19.4% of positively selected CD8+ cells also expressed CD4, and thus the provirus may reside within a dual-positive population. This dual-positive population may represent activated lymphocytes that are particularly susceptible to infection and may provide an opportunity for virus entry into the CD8+ CD4- lymphocytes in vivo.

Animals↗
PubMed1996

Virus-induced immunosuppression is linked to rapidly fatal disease in infant rhesus macaques infected with simian immunodeficiency virus.

Six newborn rhesus macaques were experimentally infected with pathogenic Simian immunodeficiency virus of macaques (SIVmac251), and three newborn macaques were infected with avirulent SIVmac1A11. The former developed rapidly fatal simian AIDS and died within 26 wk of age, whereas the latter remained clinically normal. Infant monkeys that developed rapidly progressive disease had rapid declines in CD4+ cells and were unable to mount IgG and IgA antibody responses to SIV or to an unrelated antigen, tetanus toxoid. IgM antibody responses were near normal to both SIV-specific and nonspecific antigens. Cytotoxic T lymphocyte (CTL) responses to SIV envelope were observed in animals infected with either virulent or avirulent SIV. These studies demonstrated that virulent SIVmac infection induced a rapid immunosuppression that was both SIV-specific and nonspecific in nature. The observation that virulent strains of SIV can rapidly induce a global immunosuppression provides one explanation for the rapid disease course in some HIV-infected children and supports the strategy of early and vigorous antiviral drug therapy to alter the disease course even if this does not prevent infection.

Amino Acid Sequence↗
PubMed1996

Primary and secondary Toxoplasma gondii infection in normal and feline immunodeficiency virus-infected cats.

Normal and asymptomatic feline immunodeficiency virus (FIV)-infected adult cats were inoculated orally with Toxoplasma gondii tissue cysts to assess differences in clinical disease, T. gondii serologic test results, hematologic results, and oocyst shedding. There was no difference between FIV-naive and FIV-infected cats in terms of clinical illness and duration of oocyst shedding following primary exposure. Both groups of cats developed significant decreases in neutrophil counts following primary inoculation with T. gondii; FIV-infected cats that were neutropenic prior to inoculation with T. gondii developed the most profound decreases in neutrophil numbers. Both FIV-naive and FIV-infected cats became lymphopenic during acute T. gondii infection; however, only FIV-naive cats developed lymphocytosis in the recovery stage. FIV-infected cats had lower total CD4+ and higher total CD8+ T-lymphocyte counts than FIV-naive cats prior to inoculation with T. gondii, but changes in these lymphocyte subsets were similar between groups of cats during the first several weeks after inoculation. Toxoplasma gondii infection had neither an ameliorating nor enhancing effect on T-lymphocyte subset abnormalities in FIV-infected cats during acute or chronic infection. Both groups of cats developed comparable levels of T. gondii-specific IgM and IgG antibodies and T. gondii antigen-specific lymphocyte blastogenic responses following primary inoculation. Both groups of cats were fed T. gondii tissue cysts 66 wk following primary exposure and both groups were solidly immune as evidenced by a lack of oocyst shedding and only minor changes in IgM but not IgG antibodies.

Animals↗
PubMed1995

Marrow accessory cell infection and alterations in hematopoiesis accompany severe neutropenia during experimental acute infection with feline immunodeficiency virus.

Severe neutropenia and bone marrow (BM) morphologic abnormalities occur during experimentally induced primary infection with feline immunodeficiency virus (FIV), a lentivirus biologically similar to human immunodeficiency virus (HIV). To further characterize the mechanisms involved in this acute infection model of lentivirus-induced BM suppression, peripheral blood counts, histologic BM studies, and BM culture assays were performed on 12 cats that underwent necropsy at regular intervals postinoculation (PI) with FIV Petaluma. Plasma viremia developed at week 3 PI and neutropenia was initially detected at week 6 PI. Low neutrophil counts, but normal hematocrits and platelet counts, persisted through week 12 PI. Infected BM mononuclear cells and megakaryocytes were identified by in situ hybridization assays for FIV nucleic acids in BM sections of cats that underwent necropsy at weeks 4 to 12 PI, correlating with detection of soluble FIV p24 antigen and identification of infected mononuclear and macrophage cells in BM buffy-coat cell cultures from these cats. At weeks 1.5 to 4 PI, the mean frequencies (number per 10(5) BM mononuclear cells) of erythroid progenitors (erythroid colony-forming units [CFU-E] and erythroid burst-forming units [BFU-E] and granulocyte/macrophage progenitors (CFU-granulocyte/macrophage [CFU-GM]) were increased to 508 +/- 74, 143 +/- 24, and 110 +/- 17, respectively (n = 5 cats) as compared with controls (172 +/- 24, 86 +/- 26, and 44 +/- 10; n = 3 cats; P < .02), and the percentages of progenitors in the DNA-synthetic phase of the cell cycle were equivalent to controls. In contrast, the progenitor frequencies at weeks 6 to 12 PI were significantly decreased (72 +/- 16, 43 +/- 6, and 19 +/- 4, respectively; n = 7 cats; P < .01), and these progenitors were more frequently in S-phase. Autologous serum significantly inhibited (P < .05) the growth of CFU-GM in 6 of 9 cats and failed to support the maximal growth of BFU-E in 4 of 9 cats studied at weeks 4 to 12 PI, whereas no such abnormalities were observed in colony assays containing autologous sera from control cats (n = 3) or cats studied at weeks 1.5 or 3 PI (n = 3). In comparison, sera from FIV-infected cats did not inhibit the growth of normal, allogeneic progenitors. However, FIV serum frequently failed to support maximal in vitro growth of normal CFU-GM as compared with uninfected allogeneic sera, further suggesting a lack of progenitor growth-promoting substances in infected cat sera.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗