The simian immunodeficiency virus (SIV)-rhesus macaque model of heterosexual human immunodeficiency virus transmission consists of atraumatic application of cell-free SlVmac onto the intact vaginal mucosa of mature female rhesus macaques. This procedure results in systemic infection, and eventually infected animals develop the clinical signs and pathologic changes of simian AIDS. To achieve 100%0 transmission with the virus stocks used to date, multiple intravaginal inoculations are required. The current titration study utilized two stocks of SlVmac and demonstrated that a single intravaginal dose of cell-free SIV can reliably produce infection in rhesus macaques. This study also demonstrated that some animals intravaginally inoculated with cell-free SIVmac develop transient viremia characterized by a limited ability to isolate virus from peripheral blood mononuclear cells and lymph node mononuclear cells and no seroconversion to SIV antigen. SIV could be isolated from the peripheral lymph nodes of transiently viremic animals only during periods of viremia and not at times when SIV was not detected in circulating mononuclear cells. Thus, peripheral lymphoid tissues were not reservoirs of infection in the transiently viremic animals. Taken together, these results suggest either that the SIV infection was cleared in the transiently viremic animals or that SIV infection is limited to a compartment of the genital mucosal immune system that cannot be assessed by monitoring SIV infection in peripheral blood mononuclear cells and peripheral lymphoid tissue.

Sex steroid hormones are involved in regulating the immune system [1,2] and autoimmune diseases effect women to a greater degree than men (reviewed in [3]). Multiple sclerosis and rheumatoid arthritis occur between two and three times more often in women and systemic lupus erythematosus affects nine times more women than men (reviewed in [3]). Oestrogen is the defining ovarian steroid hormone and effects of oestrogen are mediated by two distinct intracellular receptors, ER-alpha and ER-beta [4]. It seems that women have a greater susceptibility to autoimmune disease at least in part because they make stronger immune responses. The levels of IgM in a primary response, and IgG in a secondary immune response are higher in sexually competent female mice compared to male mice of equivalent age [5][6][7]. In humans, plasma IgM levels [8] and peripheral CD4 + T cell counts are higher in women than in men [9].In addition to stronger immune responses and higher concentrations of antibodies and lymphocytes, regulation of immunity is complex in females because lymphocytes respond to changing concentrations of steroid sex hormones. There is a dramatic reduction in the number of activated and committed B cell precursors in the bone marrow of pregnant mice, and this is thought to be due to the elaboration of sex steroids during pregnancy [10,11]. In mice, long-term exposure to high doses of exogenous oestradiol enhances polyclonal B cell activation [12]. In-vitro, oestrogen enhances non-specific differentiation of human immunoglobulin-secreting cells (ISCs) [13][14][15] and this oestrogen-mediated enhancement is due to inhibition of suppressor T cells [14]. It should be clear from this very brief review that ovarian steroid hormones can regulate immune cell function.Ovarian sex steroids levels have a particular influence on female genital tract immunity. In the rat, the stage of the oestrous 10The strength of B cell immunity in female rhesus macaques is controlled by CD8 + T cells under the influence of ovarian steroid hormones SUMMARYTo understand more clearly how mucosal and systemic immunity is regulated by ovarian steroid hormones during the menstrual cycle, we evaluated the frequency of immunoglobulin-and antibodysecreting cells (ISC, AbSC) in genital tract and systemic lymphoid tissues of normal cycling female rhesus macaques. The frequency of ISC and AbSC was significantly higher in tissues collected from animals in the periovulatory period of the menstrual cycle than in tissues collected from animals at other stages of the cycle. The observed changes were not due to changes in the relative frequency of lymphocyte subsets and B cells in tssues, as these did not change during the menstrual cycle. In vitro, progesterone had a dose-dependent inhibitory effect, and oestrogen had a dose-dependent stimulatory effect on the frequency of ISC in peripheral blood mononuclear cell (PBMC) cultures. The in vitro effect of progesterone and oestrogen on ISC frequency could not be produced by incubating enriched B cells alone with ho...

SUMMARY The biuret method of protein estimation was compared with the Kjeldahl method. Highly significant positive correlations with Kjeldahl protein of 0.99, 0.99, 0.98, and 0.99 were obtained for ground beef, pork, chicken breast, and cod, respectively. The high correlations between the two methods and the small standard deviations for the biuret values point out the reliability and the accuracy of the biuret method. The same substances were analyzed by the Orange G dye‐binding method with highly significant positive correlations with Kjeldahl protein of 0.90, 0.80, 0.94, and 0.95 for ground beef, pork, chicken breast, and cod, respectively. However, the amount of dye bound per g protein varies with the protein content of the sample, and the precision is poor. Orange G dye binding has possibilities for use in analyzing meat proteins only if the preparations and procedures are carefully standardized and the protein content does not vary more than a few percent. With Amido Black 10B, the amount of dye bound was too strongly dependent upon sample size to justify further investigation of this dye for estimation of the protein content of comminuted meats.

An infectious, virulence-attenuated molecular clone of simian immunodeficiency virus (SIV), SIVMAC-IA119 was derived from an SIV isolate that causes fatal immunodeficiency in rhesus macaques. When inoculated intravenously in rhesus macaques, SIVMAC IAII induced transient viremia (1 to 6 weeks) without clinical disease and a persistent humoral antibody response. The antibodies were directed mainly against the viral envelope glycoproteins, as determined by immunoblots and virus neutralization. The potential of this virulence-attenuated virus to protect against intravenous challenge with a pathogenic SIVMAC strain was assessed. Five rhesus macaques were each given two intravenous inoculations with SIVMACIAI1 7 months

The intact cervicovaginal mucosa is a relative barrier to the sexual transmission of human immunodeficiency virus type 1 (HIV-1). In the simian immunodeficiency virus (SIV) macaque model of HIV infection, seronegative transient viremia (STV; virus isolation positive followed by repeated negative cultures) occurs after intravaginal inoculation of a low dose of pathogenicSIVmac251 (C. J. Miller, M. Marthas, J. Torten, N. Alexander, J. Moore, G. Doncel, and A. Hendrickx, J. Virol. 68:6391-6400, 1994). Thirty-one adult female macaques that had been inoculated intravaginally with pathogenic SIVmac251 became transiently viremic. One monkey that had been culture negative for a year after SIV inoculation became persistently viremic and developed simian AIDS. No other STV monkey developed persistent viremia or disease. Results of very sensitive assays showed that 6 of 31 monkeys had weak SIV-specific antibody responses. SIV-specific antibodies were not detected in the cervicovaginal secretions of 10 STV monkeys examined. Twenty of 26 monkeys had lymphocyte proliferative responses to p55 gag and/or gp130 env antigens; 3 of 6 animals, including the monkey that became persistently viremic, had detectable cytotoxic T-lymphocyte (CTL) responses to SIV. At necropsy, lymphoid tissues and vaginal mucosa were virus culture negative, but in 10 of 10 animals, SIV provirus was detected by PCR using gag-specific primer pairs. Fifty percent of the PCR-positive tissue samples were also positive for SIV gag RNA by reverse transcriptase PCR. Thus, transient viremia following intravaginal inoculation of pathogenic SIV is associated with persistent, systemic infection, either latent or very low level productive. Atypical immune responses, characterized by lymphocyte proliferation and some CTL responses in the absence of conventionally detectable antibodies, develop in transiently viremic monkeys.