Sixteen isolates of simian retrovirus closely related to human immunodeficiency virus (HIV) were obtained from healthy African green monkeys (AGM) (Cercopithecus aethiops). The first isolate was obtained from a monkey seropositive for HIV, and the others were isolated from monkeys harboring antibodies to the first isolate. These simian retroviruses were referred to as simian immunodeficiency virus from AGM, SIV[AGM], due to their cross-reactivities with HIV structural proteins. These SIV[AGM] isolates were found by Western blotting analysis to have virus-specific proteins of 120, 66, 55, 32-40, 24 and 17 kDa, which were all similar in size to the analogous proteins of HIV. Putative gag proteins of p55, p24 and p17 were recognized by sera of human AIDS patients, but the corresponding env proteins of 32-40 and 120 kDa showed only weak cross-reactivity with those of HIV. The transmembrane glycoproteins of these 3 SIV[AGM] isolates showed size heterogeneity, being 32, 35 and 40 kDa. This virus had particles that were morphologically similar to those of HIV, and had Mg2+-dependent reverse transcriptase. Furthermore, the SIV[AGM] showed tropism and cytopathic effects on CD4-positive human cell lines. In a sero-epidemiological survey of SIV[AGM] in various non-human primates, 2 other African monkey species, the mandrill and de Brazza's monkey, were also found to have antibodies to SIV[AGM]. These HIV-related simian retroviruses will be important in determining the origin and transmission of HIV group viruses, and may provide useful animal models for studies on the infection and pathogenesis of HIV and AIDS.

The prevalence of adult T-cell-leukemia virus (ATLV) infection was examined in Japanese monkeys living naturally in various parts of Japan and in other species of non-human primates imported into and kept in Japan. Sera of 2,650 Japanese monkeys from 41 troops throughout Japan were tested. High incidences of anti-ATLV-associated antigen (ATLA)-positive monkeys were found in most troops, not only in the endemic area of human ATL(Southwestern Japan), but also in non-endemic areas. The incidence of sero-positive individuals increased gradually with age, reaching a maximum when the animals became adult, indicating age dependency, like that found by epidemiological studies on humans. Anti-ATLA antibodies were also detected in 90 of 815 sera of imported non-human primates of 33 species other than Japanese monkeys. All the anti-ATLA sero-positive monkeys were Catarrhines (Old World monkeys), mainly macaques of Asian origin. Some sero-positive monkeys were also found among animals of African origin, but no antibody was detected in Prosimians and Platyrrhines (New World monkeys). The clear-cut difference between the geographical distribution of sero-positive simians and that of humans indicates the improbability of direct transmission of ATLV from simians to humans.

Protection against human T-cell leukemia virus type-I (HTLV-I) infection in cynomolgus monkeys, achieved by immunizing the animals with env gene products of HTLV-I produced in Escherichia coli, was evaluated. Four monkeys that had been immunized with the env product produced antibody against HTLV-I gp68 and gp46, and their sera were found to cause strong inhibition of syncytium formation of a cat fibroblast cell line induced by HTLV-I. Immunized and non-immunized monkeys were challenged with live MT-2 cells, a high HTLV-I-producer cell line. After challenge, all the control non-immunized monkeys were infected with HTLV-I, as judged by the frequent detection of HTLV-I-antigens in cultures of their peripheral blood mononuclear cells (PBMC), whereas no antigens were recovered from PBMC of immunized monkeys. These results indicate that humoral immunity against HTLV-I-envelope protein elicited by immunization with the polypeptides synthesized in bacteria protected the monkeys against primary infection with HTLV-I.

SUMMARY : Studies on the pathogenicity of Shigella have been conducted, employing various experimental models and acid agglutination test with S. flexneri 2a strain 5503 and its variants. The parent strain 5503 isolated from a dysentery monkey behaved as a virulent one with respect to oral infectivity for monkeys, keratoconjunctival infectivity for guinea pigs, and penetration and multiplication within cultured monolayer cells, whereas variants 5503-I and 5503-II derived from strain 5503 were avirulent. Neither parenteral virulence for mice nor acid agglutinability gave consistent relation. The results obtained agreed well with those established by LaBrec et al.(1964).Localization of the dysentery bacilli and inflammatory reactions induced were followed by examining keratoconjunctivitis in guinea pigs by the fluorescent antibody and histopathological techniques.The significance in the pathogenesis of bacillary dysentery of epithelial cell penetration and intracellular multiplication of the bacilli is discussed in connection with oral infectivity for monkeys.

To determine whether sex-linked factors are important in the susceptibility and resistance of cynomolgus monkeys to type I1 collagen-induced arthritis, we immunized 5 males and 10 females with chick type I1 collagen (CII) and studied their clinical and immune responses. All 10 females developed overt arthritis and produced antibodies to CII and cross-reactive antibodies to monkey type I1 collagen (MkII). In contrast, only 1 male monkey developed arthritis, which was transient and mild in severity. Examination of antisera obtained from the male monkeys disclosed high titers of antibody to CII, but little antibody to MkII. The cyanogen bromide peptide recognition patterns varied markedly from animal to animal, implying that monkeys are capable of recognizing multiple arthritogenic determinants on CII.The observations that certain strains of rats (I-4), mice (5-9), and nonhuman primates (10,ll) develop a destructive polyarthritis after immunization with heterologous or homologous type I1 collagen have stimulated interest in the potential role that autoimmunity to collagen might play in the pathogenesis of human arthritic diseases, such as rheumatoid arthritis and relapsing polychondritis. In rodents, susceptibility to collagen-induced arthritis is closely associated with the formation of antibodies that cross-react with homologous type 11 collagen (2,4,7,12). The critical role that anticollagen antibodies play in the initiation of collagen-induced arthritis has been underscored by studies showing that this disease can be passively transferred to naive animals with purified antibodies to heterologous or homologous type I1 collagen (13-15). The recent observation that collagen-induced arthritis can be passively transferred to mice with anti-type 11 collagen antibodies purified from rheumatoid serum supports the hypothesis that anticollagen antibodies might be pathogenic in humans (16).Investigations into the location of arthritogenic epitopes on the cyanogen bromide (CB) peptides of chick type I1 collagen (CII) have shown that the CBI 1 peptide is of particular importance (17). This conclusion stems from the discovery that antibodies produced by arthritic DBAil mice immunized with native or denatured CII react most intensely with CB 11 and only variably with the other CB peptides. When tested for cross-reactivity with mouse type I1 collagen (MsII), antibodies to CB I 1 consistently showed the