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Biomedical subjects

R C Weiss

Publications and source records attributed to R C Weiss.

At least 19 recordsLinked to original sources
PubMed1992

Immunologic responses in healthy random-source cats fed N,N-dimethylglycine-supplemented diets.

The immunomodulatory capacities of N,N-dimethylglycine (DMG) were examined in random-source cats. Blood mononuclear leukocytes of healthy adult cats that had negative results to tests for FeLV and feline immunodeficiency virus were exposed in vitro to various concentrations of DMG (10 to 1,000 micrograms/ml) and were evaluated for proliferative responses to T- or B-cell phytomitogens. Although increased, mean lymphocyte blastogenic responses to phytolectins in DMG-treated cultures did not differ significantly from responses of untreated cultures. For in vivo studies, cats were given a solution containing either 100 mg of DMG or a control solution without DMG orally at 8 AM and 6 PM for 40 consecutive days. On post-treatment day 24 and 25, mean blastogenic responses to phytolectins in DMG-treated and control cats inoculated 10 days earlier with an inactivated feline virus vaccine were similar. Cats given DMG and inoculated twice in a 3-week interval with a commercial vaccine containing inactivated feline herpesvirus-1 and feline calicivirus had significantly (P = 0.045) lower virus neutralizing serum antibody titers against feline herpesvirus-1, compared with titers of control cats, whereas feline calicivirus titers were similar in both groups. On day 25, mean serum interferon activity, induced after IV inoculation of Newcastle disease virus, was significantly (P = 0.021) lower in the DMG-treated cats. Results of this study of DMG in healthy cats failed to demonstrate enhancement of either specific or nonspecific immunity.

Adjuvants, Immunologic↗
PubMed1990

The clinical and histologic appearance of HIV-associated gingivitis.

Human immunodeficiency virus-associated gingivitis (HIV-G) has been described recently as a clinical entity in HIV-infected patients. However, little is known about the etiology and pathogenesis of this condition. We report a case of HIV-G in a 32-year-old man with acquired immunodeficiency syndrome (AIDS). The histology of the clinically involved gingiva revealed the absence of an inflammatory cell infiltrate. This report provides an initial description of the histologic changes occurring in HIV-G.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Effect of recombinant human interferon-alpha in vitro and in vivo on mitogen-induced lymphocyte blastogenesis in cats.

The effect of recombinant human interferon-alpha (rHuIFN-alpha) in vitro and in vivo on mitogen-induced lymphocyte blastogenesis was evaluated in specific-pathogen-free cats. Pre-incubation of isolated feline peripheral blood lymphocytes (PBL) in vitro with either 10(4) or 10(3) International Units (U) of rHuIFN-alpha for 24 h significantly suppressed (P less than 0.001 and 0.01, respectively) blastogenic responses to the phytomitogens concanavalin A (Con A) and pokeweed mitogen (PWM). Lower doses of IFN (range, 10-10(-3) U/ml) neither suppressed nor enhanced mitogenesis. In the absence of phytomitogens, incubation of PBL with 10(4) - 10(2) U (P less than 0.001) or 10 U (P less than 0.05) of rHuIFN-alpha/ml resulted in a significant decrease in incorporation of [methyl-3H] thymidine into newly synthesized cellular DNA. Cultures of PBL exposed continuously for 4 days to rHuIFN-alpha doses of 10(4) U/ml or less did not demonstrate specific reductions in cell viability, indicating that the observed antiproliferative actions of IFN apparently were independent of any direct cytotoxic effects. To investigate the dose-response effects of rHuIFN-alpha in vivo on lymphocyte blastogenesis, individual groups of cats were evaluated on 3 consecutive days before and then 24 h after each cat was inoculated intramuscularly with either a high dose (10(6) U/kg), moderate dose (10(4) U/kg), or a relatively low dose (10(2) U/kg) of rHuIFN-alpha. Cats inoculated with 10(6) U of rHuIFN-alpha/kg had significantly reduced (P = 0.037) blastogenic responses to Con a at 24 h postinoculation compared to preinoculation values; mean PWM responses were also decreased, but this effect was not statistically significant. In contrast, inoculation of cats with either 10(4) or 10(2) U of rHuIFN-alpha/kg significantly enhanced (P = 0.05 or 0.008, respectively) Con A-induced blastogenesis and had no discernible effect on PWM responses. These findings suggest that very high doses of rHuIFN-alpha given parenterally may be associated with suppression of certain T-cell responses in cats; conversely, much lower doses may be immunoenhancing.

Analysis of Variance↗
PubMed1990

Potentiation of platelet responses in vitro by feline infectious peritonitis virus.

The effect of feline infectious peritonitis virus (FIPV) on platelet aggregation and 14C-serotonin release induced by threshold levels of four agonists (adenosine diphosphate [ADP], collagen, arachidonic acid, and epinephrine) was examined in vitro in ten specific-pathogen-free cats. Purified suspensions of FIPV added to stirred platelet suspensions (virus to platelet ratio equal to 1:320) 1 minute prior to the addition of agonist potentiated the ADP-induced aggregation response by greater than 100% in seven cats. Platelet 14C-serotonin release was increased by greater than 100% in four cats. Collagen-induced platelet aggregation was enhanced in ten cats while collagen-induced 14C-serotonin release was enhanced in eight cats. Potentiation of arachidonic acid-induced platelet aggregation was observed in three cats, two of which demonstrated enhanced platelet 14C-serotonin release. Although epinephrine-induced platelet aggregation was enhanced in five cats, the samples displayed only fine microaggregates. Enhanced 14C-serotonin release from platelets in response to epinephrine was not demonstrated. Interaction with the outer platelet membrane and internalization of viral particles within the surface-connected open canalicular system were demonstrated by electron microscopy within 5 minutes of the addition of virus to platelet suspensions with or without added agonists. Decreasing the virus concentration by ten- or one hundred-fold abolished the potentiating effect observed previously, while increasing the concentration tenfold resulted in direct platelet activation in the absence of agonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1990

Enhanced platelet reactivity in cats experimentally infected with feline infectious peritonitis virus.

Platelet function was evaluated in six specific-pathogen-free cats prior to and following intraperitoneal inoculation with feline infectious peritonitis virus (FIPV). By 4 days post-inoculation, platelet samples from five of six cats responded with irreversible platelet aggregation to threshold concentrations of adenosine diphosphate (ADP). This was accompanied by enhanced platelet 14C-serotonin release (greater than 10%) in two cats. Compared to one of six baseline samples, five of five post-inoculation samples exhibited microaggregate formation in response to 20 microM epinephrine. Enhanced platelet 14C-serotonin release did not accompany these responses. Enhanced platelet responses to ADP and epinephrine were also observed on day 11 post-inoculation and day 16 (when one cat died) or 21 (the end of the study). Platelet 14C-serotonin release in response to 20 microM epinephrine increased markedly in three of five cats on day 21. Enhanced collagen-induced platelet responses were not demonstrated. Although the mechanism for the enhanced platelet responses observed on day 4 was unknown, a direct effect on the virus on platelets, mononuclear inflammatory cells, and endothelial cells must be considered.

Adenosine Diphosphate↗
PubMed1990

Effect of interferon or Propionibacterium acnes on the course of experimentally induced feline infectious peritonitis in specific-pathogen-free and random-source cats.

Seventy-four cats (52 treated and 22 untreated) were evaluated in efficacy studies of interferon (IFN), Propionibacterium acnes, or a combination of these drugs against experimentally induced feline infectious peritonitis (FIP). Cats were given doses of recombinant human leukocyte (alpha) IFN (rHuIFN-alpha), feline fibroblastic (beta) IFN (FIFN-beta) or P acnes at regular intervals before and after inoculation of virulent FIP virus (FIPV). Prophylactic and therapeutic administration of high doses (10(6) U/kg of body weight) or moderate doses (10(4) U/kg) of rHuIFN-alpha, FIFN-beta (10(3) u/kg), or P acnes (0.4 or 4 mg) did not significantly reduce mortality in treated vs untreated cats. However, the mean survival time in cats treated with 10(6) U of rHuIFN-alpha-/kg alone or combined with doses of P acnes was significantly (P = 0.03) increased after inoculation of highly lethal amounts (200 LD100) of FIPV vs survival time in untreated cats. Although P acnes alone was ineffective, there was some indication that a combination of P acnes and high doses of rHuIFN-alpha was more effective than rHuIFN-alpha alone. Seemingly, the efficacy of rHuIFn-alpha treatment was improved in cats challenge-exposed with less FIPV; in 1 trial, 4 of 5 cats (80%) treated with high doses of rHuIFN-alpha survived after inoculation of minimal lethal amounts (0.6 LD100) of FIPV, whereas only 2 of 5 untreated cats (40%) survived. Pretreatment of cats with 10(6) U of rHuIFN-alpha/kg resulted in detectable serum IFN activity 24 hours later; serum IFN activity was not detected in cats pretreated with P acnes, FIFN-beta, or 10(4) U of rHuIFn-alpha/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adjuvants, Immunologic↗
PubMed1989

Evaluation of immunity to feline infectious peritonitis in cats with cutaneous viral-induced delayed hypersensitivity.

Delayed-type hypersensitivity (DTH)-like reactions to feline infectious peritonitis (FIP) virus (FIPV) were induced in the skin of nine cats that were asymptomatic after a previous challenge-exposure with FIPV. Four of the nine previously challenge-exposed cats were negative for virus-neutralizing antibodies against FIPV at the time of intradermal (ID) testing for DTH. Two other cats tested for DTH when acutely ill with clinical FIP did not have cutaneous DTH responses to FIPV. Gross skin reactions to FIPV injected ID were observed in six of nine asymptomatic cats (67%) at postintradermal inoculation hours (PIH) 24, 48, and/or 72. The reactions consisted of focal, 1-5-mm to 2.5-cm diameter indurated or semi-firm, nonerythematous, slightly raised nodules. Microscopically, DTH-like reactions were observed in biopsies taken from the FIPV-inoculated skin of asymptomatic cats at PIH 24 to 72. The lesions consisted of perivascular and diffuse dermal infiltrations by macrophages, lymphocytes, and polymorphonuclear leukocytes (PMN). The dermal infiltrates, which were maximal at PIH 48 or 72, were predominantly mixed inflammatory cells (five of nine cats) or PMN (four of nine cats) at PIH 24, but later were predominantly mononuclear cells (six of nine cats) or mixed inflammatory cells (two of nine cats) at PIH 72. Five of nine cats (56%) with positive DTH skin responses had increased survival times after lethal ID challenge-exposure with FIPV compared to mean survival times in FIPV-naive, non-immune control cats that were DTH-negative when ID challenge-exposed. Four of nine DTH-positive cats (44%) resisted an ID challenge-exposure dose of FIPV that was fatal in both control cats, and two of the four remaining DTH-positive cats survived a third challenge-exposure with highly lethal doses of FIPV given intraperitoneally. Four of the six DTH-positive cats (67%) that died after re-challenge and were necropsied had lesions of noneffusive FIP, suggesting that cellular immunity may also be involved in the pathogenesis of noneffusive disease, whereas both control cats and both DTH-negative cats with clinical disease succumbed to effusive FIP. Seemingly, DTH responses to FIPV can be associated with an increased level of resistance to disease; however, this state of immunity is variable and apparently can be lost with time in some cats.

Animals↗
PubMed1989

Inhibitory effects of ribavirin alone or combined with human alpha interferon on feline infectious peritonitis virus replication in vitro.

The antiviral activities of ribavirin (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide; virazole), either alone or in combination with recombinant human leukocyte (alpha) interferon (rHuIFN-alpha), were evaluated against feline infectious peritonitis virus (FIPV) in feline kidney-cell cultures. The 50% inhibitory dose (ID50) of ribavirin for uninfected, rapidly dividing cells was approximately 17 micrograms ml-1 whereas the ID50 for FIPV was 2.5 micrograms ml-1. The therapeutic index (TI) of ribavirin (i.e. the ratio of the minimum cell-toxic dose to minimum virus-inhibitory dose) was 6.8. Although a dose-dependent inhibition of viral infectivity occurred at non-toxic doses, maximum antiviral effects (greater than or equal to 4 log10 reduction in FIPV) occurred at cytotoxic doses. When low or moderate doses of ribavirin were combined with either 10 or 100 U of rHuIFN-alpha ml-1, the resulting antiviral effects were significantly greater than the sum of the observed effects from either ribavirin or rHuIFN-alpha alone. Significant synergistic interactions with rHuIFN-alpha occurred at ribavirin doses of 1, 5, 12.5 and 25 micrograms ml-1. Synergistic combinations of rHuIFN-alpha and ribavirin produced up to an 80-fold or a 200-fold relative increase in FIPV antiviral activities compared with that produced by equivalent doses, respectively, of ribavirin or rHuIFN-alpha alone. In cell growth studies, the addition of either 10 or 100 U of rHuIFN-alpha ml-1 to test doses of ribavirin did not increase the anticellular effect observed with ribavirin alone; seemingly, the potentiation of ribavirin antiviral activity by rHuIFN-alpha was independent of any additive cytotoxic effects. Potentially, synergistic combinations of the two antiviral agents in vivo may decrease the therapeutic dose of ribavirin required for inhibition of FIPV and thus reduce drug toxicity.

Animals↗
PubMed1989

Synergistic antiviral activities of acyclovir and recombinant human leukocyte (alpha) interferon on feline herpesvirus replication.

The antiviral activities of 9-(2-hydroxyethoxymethyl)guanine (acyclovir; ACV) either alone or combined with recombinant human leukocyte (alpha) A/D interferon (rHuIFN-alpha) against feline herpesvirus type 1 (FHV-1) were evaluated in feline embryo cell cultures, using an infectivity-inhibition assay. In ACV-treated cultures, the 50% inhibitory dose (ID50) was approximately 10 to 20 micrograms of ACV/ml. Maximal inhibition of FHV-1 infectivity (range, 3.4 to 4.2 log10 TCID50) was observed when high test doses of ACV (125 or 250 micrograms/ml) were given 1 to 6 hours after infection. Although mild inhibition (range, 0.3 to 1.6 log10 TCID50) of virus was observed at lower drug doses (10 to 62.5 micrograms/ml), FHV-1 was relatively resistant to ACV and required higher minimal inhibitory doses than those reported for other herpesviruses. However, when ACV was combined with 10 or 100 U of rHuIFN-alpha/ml, synergistic antiviral effects were associated with ACV dosage of 10 to 62.5 micrograms/ml. Antiviral activities resulting from use of the combined drugs permitted nearly eightfold reduction in the dose of ACV required to achieve maximal inhibition of FHV-1. Significant (P less than 0.01) synergistic interactions with ACV resulted when the rHuIFN-alpha was given before or after infection; at the lower doses of ACV, however, rHuIFN-alpha pretreatment was more effective. Although dosages of either greater than or equal to 62.5 micrograms of ACV/ml or 100 U of rHuIFN-alpha/ml were cytosuppressive in control cell cultures, additive anticellular effects were not observed at synergistic combinations of ACV and 10 U of rHuIFN-alpha/ml.

Acyclovir↗
PubMed1989

Evaluation of antithrombin-III activity as a coindicator of disseminated intravascular coagulation in cats with induced feline infectious peritonitis virus infection.

Six adult specific-pathogen-free cats were inoculated intraperitoneally with a cell culture-adapted strain of feline infectious peritonitis virus. Plasma samples were evaluated for antithrombin-III (AT-III) activities at post-inoculation days (PID) 0, 4, and 11 and at termination on PID 16 (1 cat) or 21 (5 cats). Other hemostatic values evaluated were activated partial thromboplastin times, prothrombin times, thrombin times, fibrinogen, platelet counts, and fibrin/fibrinogen degradation products. Antithrombin-III activity remained within normal or above normal range (89 to 246%) in all cats, with the exception of one cat on PID 4 (AT-III, 70%). Mean baseline AT-III activity for 6 cats at PID 0 was 123%. Mean AT-III activity on PID 4, 11, and 16 or 21 was 98, 162, and 130%, respectively. On PID 4 and 16 or 21, results of coagulation screening tests indicated that all cats had disseminated intravascular coagulation. Histologically, cats also had severe fibrinonecrotizing thrombovasculitis.

Acute Disease↗
PubMed1988

Increased plasma levels of leukotriene B4 and prostaglandin E2 in cats experimentally inoculated with feline infectious peritonitis virus.

Specific-pathogen-free kittens experimentally infected with feline infectious peritonitis virus (FIPV) subsequently demonstrated increased plasma levels of the arachidonic acid metabolites, leukotriene (LT) B4 and prostaglandin (PG) E2. Significant increases (P less than 0.025) in LTB4 plasma levels occurred in all (5/5) FIPV-inoculated kittens on postchallenge-exposure days (PCD) 7 and 14 vs PCD 0. Significant increases (P less than 0.05) in PGE2 plasma levels occurred in 80% (4/5) of FIPV-infected kittens on PCD 7 and 14. Maximal mean plasma levels of LTB4 and PGE2 occurred on PCD 7 (502.5 +/- 45.6 pg/ml and 1108.0 +/- 247.9 pg/ml, respectively). A positive correlation was found between LTB4 plasma levels and body temperature (r = 0.609, P less than 0.01). Mean survival time in FIPV-inoculated kittens was 19.4 +/- 3.2 days. Gross lesions, including peritoneal or pleural effusions (or both) and connective tissue edema, indicated an increased vascular permeability in the FIPV-infected kittens. Histologically, lesions were characterized by vasculitis or perivasculitis, vasodilatation, perivascular edema, and fibrinonecrotizing and pyogranulomatous inflammation. Immunofluorescent studies of tissues from FIPV-infected kittens demonstrated foci of polymorphonuclear leukocytes and FIPV-positive macrophages oriented around dilated blood vessels. Seemingly, arachidonic acid metabolites, including LTB4 or PGE2 released from macrophages, neutrophils or other cells, may be involved in the pathogenesis of FIP vascular and inflammatory lesions and in some of the clinical disease manifestations.

Animals↗
PubMed1988

Delayed-type hypersensitivity skin responses associated with feline infectious peritonitis in two cats.

Two cats previously challenge-exposed and seropositive to feline infectious peritonitis virus (FIPV) were evaluated for delayed-type hypersensitivity (DTH) skin responses to intradermal FIPV. Before testing, cat 1 (FIP-resistant) had survived a severe experimental FIPV challenge-exposure and had remained asymptomatic, whereas cat 2 (FIP-susceptible) developed acute fulminant FIP after a considerably smaller virus challenge-exposure. Cat 1 developed a focal thickened plaque at the FIPV-injected skin site at 48 hours after injection. Histological examinations of serial punch biopsies from virus-inoculated skin revealed perivascular and diffuse dermal infiltrations of macrophages, lymphocytes and polymorphonuclear leucocytes which were maximal at 48 to 72 hours after injection. In contrast, cat 2 did not react grossly and showed only very mild dermal infiltrates at 72 hours after injection. The present findings of strong DTH responses to FIPV in a resistant cat and minimal responses in a cat with acute fulminant FIP suggest that certain in vivo cellular immune reactions may be associated with disease resistance.

Animals↗
PubMed1988

Inhibition of feline infectious peritonitis virus replication by recombinant human leukocyte (alpha) interferon and feline fibroblastic (beta) interferon.

Replication of feline infectious peritonitis virus (FIPV) in feline cell cultures was inhibited after incubation of cells with either human recombinant leukocyte (alpha) interferon (IFN) or feline fibroblastic (beta) IFN for 18 to 24 hours before viral challenge exposure. Compared with virus control cultures, FIPV yields were reduced by ranges of 0.1 to 2.7 log10 or 2 to 5.2 log10 TCID50 in cultures treated with human alpha- or feline beta-IFN, respectively; yield reductions were IFN dose dependent. Sensitivity to the antiviral activities of IFN varied with cell type; feline embryo cells had greater FIPV yield reductions than did similarly treated feline kidney or feline lung cells. Comparison of the virus growth curves in IFN-treated and virus control cultures indicated marked reduction in intracellular and extracellular FIPV in IFN-treated cultures. Compared with virus control cultures, intracellular and extracellular infectivity in IFN-treated cultures was delayed in onset by 12 and 30 hours, respectively, and FIPV titers subsequently were reduced by 3 to 3.5 and 5 log10 TCID50, respectively. Frequently, immunofluorescent and electron microscopy of IFN-treated cells or cell culture fluids did not reveal virus; however, even in cultures without viral cytopathic changes, small amounts of virus occasionally persisted in cells.

Animals↗