Search PubMed⌕ Search

Biomedical subjects

G B Baskin

Publications and source records attributed to G B Baskin.

At least 37 records · Page 2Linked to original sources
PubMed1997

Ontogenetic and phylogenetic evaluation of the presence of fibrin-type fibrinoid in the villous haemochorial placenta.

The hypothesis that fibrin type fibrinoid deposition on villi is unique to the term human placenta was tested. Bright-field microscopy was used to examine sections of first and second trimester human placental villi and tissues from three animal species that have villous haemochorial placentae similar to the human: the armadillo, the baboon and the rhesus. Sections stained with haematoxylin and eosin showed fibrin type fibrinoid deposits were hypocellular, eosinophilic masses attached to the surface of villi examined from both the human and the animal species. The deposits were located at discontinuities in the syncytiotrophoblast layer, and the fibrinoid provided a matrix for trophoblast re-epithelization of the villous surface. It is concluded that fibrin-type fibrinoid is not unique to the term human placenta. The presence of the syncytiotrophoblast discontinuities associated with the fibrinoid deposition must be considered in models of maternal-fetal exchange in the villous haemochorial placenta.

Animals↗
PubMed1997

Cyclosporin A modulation of early virologic and immunologic events during primary simian immunodeficiency virus infection in rhesus monkeys.

Virologic and immunologic effects of immunomodulation during primary simian immunodeficiency virus (SIV) infection were examined in monkeys treated with cyclosporin or vehicle for 32 days beginning 5 days before SIV inoculation. Duration of antigenemia decreased in 5 of 7 treated monkeys, 2 having delayed onset and peak of antigenemia. Although proviral DNA levels in blood and lymph nodes and infected cell numbers in lymph nodes were transiently decreased, levels were similar to those in controls by day 14. The CD4:CD8 ratio and percentage of CD4+ CD29+ cells decreased in controls 14 days after inoculation, but this decrease was delayed in treated monkeys. Two treated monkeys demonstrated rapid disease, with progressive antigenemia preceding early deaths 90-96 days after inoculation. Nevertheless, immunomodulation influenced the kinetics of primary SIV infection in some monkeys, supporting the rationale of careful exploration of the strategy of interference with the heightened state of cellular activation together with direct antiretroviral therapy in human immunodeficiency virus infection.

Animals↗
PubMed1997

Correlation of major histocompatibility complex with opportunistic infections in simian immunodeficiency virus-infected rhesus monkeys.

The role of the major histocompatibility complex (MHC) in the pathogenesis of AIDS is complex because of compounding variables within the virus, host, and environment. Important variables can be controlled by using the experimental animal model of AIDS induced by simian immunodeficiency virus in rhesus monkeys (Macaca mulatta). We studied whether the MHC type influenced which opportunistic infections arose in an individual monkey. Several associations were found. For example, cytomegalovirus was strongly associated with Mamu-B6 (p < 0.001), whereas Cryptosporidium was associated strongly with Mamu-DR3 (p < 0.001). We also found that having one opportunistic infection increased the risk of having another.

Alleles↗
PubMed1996

Temporal association of interferon-alpha and p27 core antigen levels in sera of simian immunodeficiency virus infected monkeys.

We report the temporal association of interferon (IFN) and p27 core antigen production during experimental simian immunodeficiency virus Delta B670 (SIV) infection in rhesus monkeys. Peak serum IFN-alpha levels (10(2.8-5.0)U/ml) occurred 10 days post infection (p.i.) and peak p27 levels (3.1-34.4 ng/ml) occurred 10-14 days p.i. Acid-stable IFN-alpha (10(1.6-2.5)U/ml) was detected 3-5 days before p27 in sera from three monkeys and was detected with p27 (0.06-3.06 ng/ml) in four monkeys during the primary infection. Serum IFN-alpha and p27 levels became undetectable 24-40 days p.i. Two monkeys remained asymptomatic for SIV after the primary p27 antigenaemia, three monkeys had recrudescent (3-4 months p.i.) acid stable interferonaemias (10(1-2.5)U/ml) with p27 antigenaemias (0.06-2.7 ng/ml) that persisted until death, and two monkeys had acute SIV infections (died < or = 7 months p.i.) with persistent acid-stable interferonaemia (10(1.6-2.5)U/ml) and p27 antigenaemia (6-9 ng/ml). Our results indicate that the detection of acid-stable IFN-alpha in serum is closely associated with detection of p27 (P = 0.0001) and suggest that detection of acid-stable IFN-alpha and p27 core antigen is indicative of active SIV infection.

Animals↗
PubMed1996

Cryptosporidiosis of the conjunctiva in SIV-infected rhesus monkeys.

Cryptosporidium was found on the conjunctiva of 6 SIV-infected immunodeficient rhesus monkeys. Some affected membranes were inflamed. The conjunctiva is a newly recognized site for disseminated Cryptosporidium infection in spontaneously infected immuno-deficient mammals, and clinicians and investigators should be aware of its possible presence in immunodeficient patients with disseminated cryptosporidiosis.

Animals↗
PubMed1995

Distribution of SIV in lymph nodes of serially sacrificed rhesus monkeys.

Rhesus monkeys were inoculated with SIVDeltaB670 and sacrificed 2, 4, 8, and 24 weeks after inoculation or when moribund. Two monkeys predicted to have a rapid disease course and two predicted to have a slower disease course were sacrificed at each time point. Lymph nodes were studied by histopathology, immunohistochemistry, in situ hybridization, electron microscopy, flow cytometry for lymphocyte subsets, and mitogen responsiveness. A greater selective decrease in peripheral CD4+CD29+ (helper-inducer/memory) T cells occurred in monkeys with high antigenemia. Although the percentage of CD8+ lymphocytes was increased and the CD4+/CD8+ ratio decreased in all infected groups, there were no consistent differences between monkeys with high or low antigenemia in lymph node lymphocyte subsets. Blastogenic responses of lymph node lymphocytes to PHA, ConA, or PWM were not significantly altered in infected monkeys. A reticular pattern typical of antigen deposition within germinal center follicular dendritic cells was seen in three monkeys with atrophic lymph nodes, high serum antigenemia, and a low percentage of circulating CD4+/CD29+ cells. More individually stained cells were in monkeys with high serum antigen and in moribund animals. By in situ hybridization, most monkeys had signal in a reticular pattern of germinal centers. Animals with higher levels of serum antigenemia tended to have more infected cells and a more intense signal. Extracellular virions were found between the FDC foot processes in the germinal centers of lymph nodes. Disease course was already established 2 weeks after inoculation.

Animals↗
PubMed1995

Squamous epithelial proliferative lesions associated with rhesus Epstein-Barr virus in simian immunodeficiency virus-infected rhesus monkeys.

Proliferative lesions were found on the squamous epithelium of the tongue, esophagus, or penis or haired skin of the lip, hand, or thorax of 8 simian immunodeficiency virus-infected rhesus monkeys that died of simian AIDS. The lesions were focal and consisted of hyperkeratosis, parakeratosis, and acanthosis in the skin, with additional ballooning degeneration in the tongue, esophagus, and penis. The epithelial surfaces were frequently colonized by Candida species or gram-positive cocci. Intranuclear inclusion bodies were seen in cells in the middle and superficial layers. Herpesvirus virions were found in inclusion-bearing cells by transmission electron microscopy. An Epstein-Barr-like virus was identified in inclusion-bearing cells by immunohistochemistry and in situ hybridization. No virus was detectable in basal layers of the epithelium. These lesions resemble oral hairy leukoplakia in AIDS patients and may thus provide a useful primate model to study permissive epithelial infection by Epstein-Barr-like viruses.

Animals↗
PubMed1995

Experimental leprosy in monkeys. I. Sooty mangabey monkeys: transmission, susceptibility, clinical and pathological findings.

A total of 31 sooty mangabey monkeys (SMM) (Cercocebus torquatus atys) inoculated by various routes with differing numbers of SMM-origin Mycobacterium leprae (ML) and 4 SMM inoculated with human-origin ML were observed for 4-12 years. SMM-origin ML was more pathogenic in SMM than human-origin ML. The spectrum of disease ranged from indeterminate to borderline and lepromatous in different animals. Some animals developed pure neural leprosy. Erythema nodosum leprosum (SNL) was also observed. Combined intravenous/intracutaneous (IV/IC) routes of inoculation more effectively induced advancing, disseminated lepromatous forms of leprosy; IV or IC routes alone were less effective at comparable doses. Total IV/IC doses of SMM-origin ML equal to or greater than 5 x 10(8), with morphologic indices (MIs) ranging from 5 to 10%, produced advancing, disseminated LL leprosy in 92% of SMM. Lower IV/IC doses and inoculations by a single IV or IC route produced fewer leprosy infections and more spontaneous regressions. As a species, captive SMM are highly susceptible to experimental leprosy and provide an excellent model for the longitudinal study of leprosy.

Animals↗
PubMed1995

Experimental leprosy in monkeys. II. Longitudinal serological observations in sooty mangabey monkeys.

In this study, 11 SMM were grouped and inoculated with differing doses of SMM-origin Mycobacterium leprae (ML) between 4.5 x 10(8) and 1 x 10(9) by either combined IV/IC routes or by IV or IC route alone. The combined route was the most effective in eliciting progressive, disseminated LL leprosy. In all, 6 of 7 SMM inoculated by the combined routes developed leprosy requiring treatment at some point. Only 1 of 4 inoculated by a single route developed persisting leprosy requiring chemotherapy. Either no disease or spontaneous regression of initial disease occurred in the other 3 animals inoculated by a single route. Doses in excess of 1 x 10(9) ML were more effective than lesser doses. An association was observed between the development of IgG anti-PGL-I ELISA OD values and resistance to leprosy and between IgM anti-PGL-I and leprosy progression or susceptibility. Serum PGL-I antigen levels, determined by dot ELISA, paralleled disease severity longitudinally. High positive OD values of anti-LAM IgG prior to ML inoculation were observed in the majority of leprosy-susceptible SMM in contrast to negative levels in more resistant animals. Anti-LAM IgG OD values exceeded the positive cut-off point after inoculation in 5 of 11 SMM; 3 of these 5 had concurrent detectable serum levels of PGL-I antigen.

Animals↗
PubMed1993

Neonatal disease induced by SIV infection of the rhesus monkey (Macaca mulatta).

Seven 72-hr-old Indian origin rhesus monkeys (Macaca mulatta) were inoculated with 10 animal ID50 of SIV/DeltaB670. Nine age-matched animals were used as uninoculated controls. All seven inoculated animals became infected as verified by viral isolation and SIV p26 antigenemia. Five of seven infected animals died within a mean of 31 days (range, 26-41 days), with high levels of antigenemia beginning 1-2 weeks postinoculation (PI) that persisted until death. Absolute lymphocyte numbers were within normal limits in all animals in both groups throughout the study. Inoculated animals that died within a mean of 31 days (short-term survivors) had significantly lower numbers of CD4+CD29+ (helper/inducer) lymphocytes than did long-term surviving inoculated animals through 3 weeks PI. Numbers of CD4+ lymphocytes were no different when controls were compared to all inoculated animals through 4-5 weeks PI. The two inoculated animals surviving 216 and 423 days PI (long-term survivors) did demonstrate declining CD4+ cells, but only late in disease. CD8+ lymphocytes were significantly lower in short-term survivors when compared to long-term survivors through 5 weeks PI. Antibody production against SIV viral proteins was detected only in the long-term survivors and was similar to results from past studies in juveniles. Clinical signs in the inoculated group were consistent with those seen in past studies on older animals. Persistent bacterial infections, primarily of the GI and respiratory tracts, were seen in the infected group. Aside from the lack of some opportunistic infections such as cytomegalovirus (CMV) and Pneumocystis carinii, necropsy findings were not different when compared to past studies on juvenile animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effects of initiation of 3'-azido,3'-deoxythymidine (zidovudine) treatment at different times after infection of rhesus monkeys with simian immunodeficiency virus.

The effects of initiating treatment with 3'-azido-3'-deoxythymidine (zidovudine) at different times after inoculation of simian immunodeficiency virus (SIV) were investigated in rhesus monkeys. Zidovudine treatments of 100 mg/kg/day (25 mg/kg, subcutaneously every 6 h) were initiated 1, 8, 24, or 72 h after intravenous inoculation of 10 ID50 of SIV. Treatments continued for 28 days, and results were compared with those of saline-treated controls. Serum infectious virus titers 14 days after inoculation (AI) significantly decreased after treatment initiation 1, 8, or 24 h AI. Titers were correlated with the time treatment was initiated. Treatments initiated 1-72 h AI prevented the establishment of persistent SIV antigenemia; greater effects were observed with earlier initiation of treatment. Treatments initiated 1-8 h AI resulted in decreased levels of viral antigenemia 14 days AI and delayed decreases in CD4+CD29+ blood lymphocytes. Earlier treatment initiation resulted in delayed recurrence of antigenemia, with a tendency for longer survival. Early initiation of treatment may be important for limiting initial viral replication and dissemination in cases of known exposure.

Animals↗
PubMed1991

Efficacy of SIV/deltaB670 glycoprotein-enriched and glycoprotein-depleted subunit vaccines in protecting against infection and disease in rhesus monkeys.

Immunization with an inactivated whole-virus vaccine is highly effective in preventing lentivirus infection. The viral protein(s) essential to the induction of protective responses, however, have not been identified. To define the role of virion components in the induction of protective immunity, we evaluated the efficacy of glycoprotein-enriched and glycoprotein-depleted simian immunodeficiency virus (SIV) subunit vaccines prepared by lentil-lectin affinity chromatography of gradient-purified virions using the immunization and challenge regimen previously found successful with an inactivated whole-virus vaccine. Infection was determined by successful recovery of virus, the induction of SIV-specific antibody responses, and infection of naive recipients by inoculation with lymph-node-derived lymphocytes from the vaccinates. Immunization with the glycoprotein-enriched preparation prevented infection in two out of four monkeys, whereas the glycoprotein-depleted vaccine failed to prevent infection in all four vaccinates tested. However, the glycoprotein-depleted vaccine appeared to moderate the progression of SIV-induced disease compared with non-immunized infected control monkeys inoculated with the same challenge dose. These data suggest that subunit vaccines containing sufficient quantities of viral glycoproteins can protect against SIV infection, whereas subunit vaccines composed predominantly of viral core proteins cannot. The development of effective vaccines against HIV infection should include studies on the optimum presentation of the viral envelope glycoproteins to produce long-term broadly protective immune responses.

Animals↗
PubMed1991

Lentivirus-induced pulmonary lesions in rhesus monkeys (Macaca mulatta) infected with simian immunodeficiency virus.

Necropsy reports from 28 rhesus monkeys that had been experimentally infected with simian immunodeficiency virus (SIV) and that were free of cytomegalovirus were reviewed. Lung sections from 24 of these monkeys that had no etiologic agent other than SIV detected in the lung were studied in detail by histopathologic, immunohistochemical, and electron microscopic examination and by in situ hybridization. Fourteen of the monkeys were part of a serial euthanasia study, while others were euthanatized after they became moribund. The following lesions were detected: perivascular inflammation, vasculitis, interstitial pneumonia, syncytial cells, hemorrhage, fibrin exudation, and pleural fibrosis. Perivascular inflammation was the most frequent lesion and occurred as early as 2 weeks after inoculation. Severe pneumonia and numerous syncytial cells were seen only in animals euthanatized because they had become moribund. The lesions appeared to be directly due to SIV infection. SIV antigens, RNA, and virions were detected in syncytial cells and macrophages by immunohistochemical examination, in situ hybridization, and transmission electron microscopic examination, respectively. The amount of virus present was correlated with the severity of the lesions. The SIV-induced lesions were different from those of the lymphocytic interstitial pneumonia, which occurs in human immunodeficiency virus-infected children and in ovine lentivirus-infected sheep and goats.

Animals↗
PubMed1991

Naturally acquired and experimental leprosy in nonhuman primates.

Naturally-acquired leprosy has been observed in chimpanzees and sooty mangabey monkeys. Experimental multibacillary leprosy was established in 24 of 36 mangabey monkeys, 7 of 34 rhesus monkeys, and 15 of 19 African green monkeys following intravenous and intradermal inoculation of Mycobacterium leprae. The experimental disease strongly resembles leprosy in humans clinically, histopathologically, and immunologically. Thus, in addition to nine-banded armadillos in Louisiana and Texas, chimpanzees and sooty mangabeys in Africa, in the wild or in captivity, may serve as a zoonotic source of M. leprae. Investigators using chimpanzees and monkeys should be alerted to the possibility of naturally-acquired leprosy.

Animals↗
PubMed1991

Experimental borderline lepromatous leprosy with intraneural erythema nodosum leprosum in a mangabey monkey (Cercocebus atys).

A sooty mangabey monkey (Cercocebus atys) was inoculated with Mycobacterium leprae and developed borderline lepromatous leprosy and intraneural erythema nodosum leprosum. Previously studied mangabeys have developed only disseminated lepromatous leprosy without reactions. This case broadens the spectrum of leprosy seen in experimentally inoculated animals and further characterizes the nonhuman primate model of leprosy.

Animals↗
PubMed1991

Disseminated histoplasmosis in a SIV-infected rhesus monkey.

Disseminated histoplasmosis due to Histoplasma capsulatum was diagnosed in a rhesus monkey inoculated with simian immunodeficiency virus (SIV). Immunohistochemical staining of tissues for viral core antigens revealed that those macrophages that expressed viral antigen contained few or no fungal organisms, while those that were filled with fungal organisms did not express viral antigen. This is a previously undocumented condition in a SIV-infected macaque, and suggests that SIV infection of individual macrophages is not the cause of macrophage dysfunction in SIV infections.

Animals↗