Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Saimiri”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1992

Platelet kinetics and other hematological profiles in experimental Plasmodium falciparum infection: a comparative study between Saimiri and Aotus monkeys.

Levels of platelets and other hematological values were monitored in 21 Saimiri and 12 Aotus monkeys over a period of three weeks post-infection with monkey-adapted Indochina CDC-1 strain of Plasmodium falciparum. In both Saimiri sciureus boliviensis and Aotus nancymai karyotype-1 monkeys the severest thrombocytopenia was observed at 14 days post-infection coinciding with peak parasitemia, neutropenia, lymphocytosis, and anemia associated with severe hemoglobinemia and elevated fibrinogen degeneration products(FDP's). MCH and MCV profiles in Aotus monkeys decreased with ascending parasitemia. In contrast, these parameters in Saimiri were characterized by a significant compensatory increase correlating with parasitemia. In general, thrombocytopenia was one of the earliest clinical manifestations of the infection with the platelets returning to normal levels shortly after peak parasitemia at 14 days. Platelet kinetics had a strong correlation with hematologic and parasitologic values in the Aotus model. No consistent associations were observed between platelet kinetics and other parameters in the Saimiri model. These data indicate that the Aotus model for malaria is more predictable than the Saimiri. Further, platelet turnover rates and recovery provide a useful prognostic parameter during malaria infection. The results are discussed in relation to the value of the two species of monkeys as models for the pathogenesis of human malaria.

Animals↗
PubMed1996

Sporozoite transmission of three strains of Plasmodium knowlesi to Aotus and Saimiri monkeys.

Attempts were made to infect Aotus and Saimiri monkeys with sporozoites of 3 strains of Plasmodium knowlesi to determine the potential of these animals in a monkey/malaria model. Splenectomized Saimiri and Aotus monkeys were infected with the H strain of P. knowlesi via sporozoites from Anopheles dirus mosquitoes. Prepatent periods ranged from 5 to 16 days. Saimiri monkeys infected with the Philippine strain had prepatent periods ranging from 6 to 8 days. Saimiri monkeys infected with the Hackeri strain had prepatent periods ranging from 6 to 11 days. Exoerythrocytic (EE) stages of the Philippine strain were readily demonstrated; EE stages of the H strain were less abundant. Results indicate that the Philippine strain of P. knowlesi in Saimiri monkeys has a course of parasitemia and EE stages similar to those previously seen in macaques and could serve as a reproducible model for biologic and immunologic studies.

Animals↗
PubMed1985

A transcription enhancer in the Herpesvirus saimiri genome.

Herpesvirus saimiri, an oncogenic agent of New World primates, has a linear double-stranded DNA genome of approximately 155 kb. To test its genome for the presence of a transcription enhancer, we have mixed randomly fragmented H. saimiri DNA with non-infectious, linear SV40 DNA lacking the 72-bp repeat enhancer region (the so-called SV40 enhancer trap) and co-transfected this DNA mixture into monkey CV-1 cells. Viable SV40-like viruses were generated by intracellular ligation/repair processes with short H. saimiri DNA fragments. One recombinant, SVHS-2, had integrated a 377-bp enhancer segment from the righthand region of the H. saimiri genome, 7 kb upstream of DNA sequences encoding an immediate-early mRNA. This enhancer sequence is contained within the non-repetitive portions of the viral genome known to be preserved episomally in all lymphoid tumor cell lines. Further recombinant viruses (SVHS-14, SVHS-7, and SVHS-8) essentially contain subsets of the 377-bp insert. Unlike in the previous enhancer trap experiments, where heterologous enhancers were incorporated without any sequence alterations, SVHS-14 and SVHS-7 have suffered short internal deletions of a very similar segment of the H. saimiri insert. This renders the enhancer more active, implying that the deleted segment, while it may have a role in the herpesvirus infection cycle, exerts a negative effect within the isolated enhancer.

Antigens, Viral, Tumor↗
PubMed1995

Induction of a herpesvirus saimiri small RNA AU binding factor (AUBF70) activity and lymphokine mRNAs by T cell mitogens.

Herpesvirus saimiri (H. saimiri) can transform T lymphocytes and cause lymphoid tumors in rabbits and New World monkeys. H. saimiri-immortalized T cells express IL-2 and IL-4. The putative oncogenes of a group C strain of H. saimiri have been mapped to a region of the unique L-DNA which includes genes encoding four U-like small nuclear RNAs (HSUR1-HSUR4). Jurkat T cells express a 70 kD RNA binding factor (AUBF70) which binds HSUR2. Here we examined AUBF70 expression in resting and mitogen-stimulated human peripheral blood T cells and its sequence specificity and subcellular distribution. Band-shift assays demonstrated that resting human T cells express low amounts of AUBF70 which is induced by mitogen treatment. IL-2 and IL-4 mRNAs were co-induced with AUBF70 suggesting that AUBF70 is a positive regulator of lymphokine gene expression. Normal resting, mitogen-stimulated, and leukemic Jurkat T cells all express AUBF70 with virtually identical V8 proteolytic enzyme digestion patterns. Northern blots demonstrated that HSUR1 and HSUR2 are localized both in the nucleus and cytoplasm. HSUR2 accumulate in the cytoplasm in the presence of actinomycin D, which is consistent with re-transport of HSURs to the nucleus by (an) unstable factor(s). We hypothesize that HSUR1 and 2 transport AUBF70 from the cytoplasm to the nucleus; in the nucleus, AUBF70 binds and stabilizes lymphokine transcripts. Increased stability of lymphokine mRNAs could contribute to oncogenic transformation induced by H. saimiri.

Base Sequence↗
PubMed2000

T cell transformation with Herpesvirus saimiri: a tool for neuroimmunological research.

The finite life span of human T lymphocytes and their requirement of regular restimulation frequently limit human T cell studies. Once infected with H. saimiri, however, human and monkey T cells are transformed to stable growth without the need for further restimulation. H. saimiri persists in human growth-transformed T cells episomally and only a few viral genes are expressed. The release of infectious virus from transformed human T cells has not been observed. H. saimiri-transformed T cells have the phenotype of mature activated CD4+ or CD8+ T cells. Transformed T cells retain a structurally and functionally intact T cell receptor and respond specifically to recognition of their antigen. They produce Th1-like cytokines, provide B cell help, can be triggered to become cytotoxic, and are sensitive to a variety of apoptosis-inducing treatments. While H. saimiri-transformed T cells resemble native T cells in numerous aspects, their reactivity to CD2 is strikingly different: Native T cells are activated via CD2 by certain pairs of mAbs, but not by the mere binding of CD2 to its ligand CD58. In contrast, H. saimiri-transformed T cells are activated by a single crosslinked anti-CD2 mAb and also by interaction with CD58-bearing cells.

Apoptosis↗
PubMed2001

Herpesvirus saimiri replaces ZAP-70 for CD3- and CD2-mediated T cell activation.

The protein tyrosine kinase ZAP-70 plays a pivotal role involved in signal transduction through the T cell receptor and CD2. Defects in ZAP-70 result in severe combined immunodeficiency. We report that Herpesvirus saimiri, which does not code for a ZAP-70 homologue, can replace this tyrosine kinase. H. saimiri is an oncogenic virus that transforms human T cells to stable growth based on mutual CD2-mediated activation. Although CD2-mediated proliferation of ZAP-70-deficient uninfected T cells was absent, we could establish H. saimiri-transformed T cell lines from two unrelated patients presenting with ZAP-70 deficiencies. In these cell lines, CD2 and CD3 activation were restored in terms of [Ca(2+)](i), MAPK activation, cytokine production, and proliferation. Activation-induced tyrosine phosphorylation of zeta remained defective. The transformed cells expressed very high levels of the ZAP-70-related kinase Syk. This increased expression was not observed in the primary T cells from the patients and was not due to the transformation by the virus because transformed cell lines established from control T cells did not present this particularity. In conclusion, wild type H. saimiri can restore CD2- and CD3-mediated activation in signaling-deficient human T cells. It extends our understanding of interactions between the oncogenic H. saimiri and the infected host cells.

Autocrine Communication↗
PubMed1981

Infection of multiple T-cell subsets and changes in lymphocyte functions associated with Herpesvirus saimiri infection of owl monkeys.

We examined the association of Herpesvirus saimiri with lymphocyte subsets and the functional integrity and distribution of these populations in owl monkeys with chronic, disease-free infections, in uninoculated, control animals, and in one monkey with H. saimiri-induced lymphoma. The lymphocyte subpopulations examined included total T cells, T cells with receptors for the Fc portion of immunoglobulin G (the Tgamma cells), T cells lacking this receptor (the Tgamma(-) population), and non-T cells. These studies showed that in chronically infected monkeys, H. saimiri was found in both Tgamma and Tgamma(-) populations and that the relative distribution of lymphocyte subsets was not different than the relative distribution in normal animals. The peripheral blood of the one leukemic animal studied showed an increase in total T cells, and both Tgamma and Tgamma(-) cells were increased in number and contained recoverable H. saimiri. In animals with chronic infections, which previously were thought to be immunologically normal, we showed that the Tgamma cells had lost the ability to respond to phytohemagglutinin. When the level of nonspecific cytotoxic activity was examined, we found that the lymphocytes from infected animals were as active as those from uninfected monkeys and that this activity was maintained at normal levels during disease. In the leukemic blood there was a relative increase in the cytotoxic activity of the Tgamma(-) cells. The Tgamma(-) cells obtained from leukemic blood lacked the ability to respond to phytohemagglutinin and could suppress the phytohemagglutinin response of normal cells. This suppressor cell activity was resistant to 3,000 rads of X irradiation. We also found that cells reactive to H. saimiri antigens could be demonstrated in the lymph nodes but not in the peripheral circulation of the lymphomatous monkey.

Animals↗
PubMed1977

Episomal viral DNA in a Herpesvirus saimiri-transformed lymphoid cell line.

The lymphoid cell line #1670 has been derived from the infiltrated spleen of a tumor-bearing marmoset monkey infected with Herpesvirus saimiri. The cells contain both types of H. saimiri DNA, unique light (L-) DNA (36% cytosine plus guanine) and repetitive heavy (H-) DNA (71% cytosine plus guanine), without producing infectious virus. Viral DNA was found to persist in these cells as nonintegrated circular DNA molecules. Closed circular superhelical viral DNA molecules were isolated by three subsequent centrifugation steps: (i) isopycnic centrifugation in CsCl, (ii) sedimentation through glycerol gradients, and (iii) equilibrium centrifugation in CsCl-ethidium bromide. The isolated circles had a molecular weight of 131.5 +/- 3.6 x 10(6). This is significantly higher than the molecular weight of linear DNA molecules isolated from purified H. saimiri virions (about 100 x 10(6)). Partial denaturation mapping of circular molecules from #1670 lymphoid cells showed uniform arrangement of H- and L-DNA sequences in all circles. All denatured molecules contained two L-DNA regions (molecular weights of 54.0 +/- 1.8 x 10(6) and 31.5 +/- 1.3 x 10(6)) and two H-DNA regions (molecular weight of 25.6 +/- 1.9 x 10(6) and 20.0 +/- 0.8 x 10(6)) of constant length. Maps of both L-regions suggested that the sequences of the shorter L-DNA region were a subset of those of the longer region. The sequences of both L-regions had the same orientation. Circular molecules from H. saimiri-transformed lymphoid cell line #1670 appeared to represent defective genomes, containing only 75% of the genetic information present in L-DNA of H. saimiri virions.

Animals↗
PubMed1986

Nononcogenic deletion mutants of herpesvirus saimiri are defective for in vitro immortalization.

Herpesvirus saimiri L-DNA sequences between 0.0 and 4.0 map units (4.5 kilobase pairs) are required for oncogenicity; these sequences are not required for replication of the virus. To investigate the basis for the lack of oncogenicity of mutants with deletions in this region and to study the function of this region, we developed a reliable system for in vitro immortalization by herpesvirus saimiri. In contrast to peripheral blood lymphocytes from cotton-top tamarins (Saguinus oedipus) and owl monkeys (Aotus sp.), infection of peripheral blood lymphocytes from common marmosets (Callithrix jacchus) in vitro with herpesvirus saimiri consistently yielded continuously growing lymphoblastoid cell lines. Such cell lines were established using strains of herpesvirus saimiri from group A and group non-A, non-B; however, repeated attempts to immortalize common marmoset peripheral blood lymphocytes using strains from group B were not successful. Common marmoset cell lines immortalized by herpesvirus saimiri were T12+, T8+, T4-, and B1-, indicating that they were derived from suppressor/cytotoxic T lymphocytes. Cell lines could not be established using the nononcogenic mutants 11att and S4, both of which were derived from the group A strain 11 virus. Strain 11att has a spontaneous deletion and S4 has a constructed deletion in the 0.0 to 4.0 map unit region. Constructed strains which had these deleted sequences restored did immortalize common marmoset peripheral blood lymphocytes. Thus, the nononcogenic deletion mutants are defective for immortalization. This system should facilitate attempts to define the sequences responsible for immortalization and to determine their function.

Animals↗
PubMed1986

Organization of the thymidylate synthase gene of herpesvirus saimiri.

Herpesvirus saimiri codes, unlike most other herpesviruses, for a thymidylate synthase (TS). The TS gene of herpesvirus saimiri is unusual in structure and regulation of expression. It is transcribed into a nonspliced mRNA of 2,190 nucleotides. The single open reading frame of the viral TS gene, instructing a polypeptide of 33.5 kilodaltons, has extensive sequence homology with the corresponding TS coding sequences of human cells and of various procaryotes; the putative polypeptide derived from the nucleotide sequence of the herpesvirus saimiri TS gene is 70% identical with the human enzyme. The untranslated regions of the herpesvirus saimiri TS gene do not share homology with the other characterized eucaryotic or bacterial TS genes. The 5' untranslated sequence has 22 ATG triplets shortly followed by stop codons. The herpesvirus saimiri TS gene, which may be weakly transcribed during immediate early and early times of virus replication, is maximally expressed at the late phase. Various parameters suggest that the TS gene has been acquired in virus evolution by an ancestral herpesvirus from the cellular genome.

Amino Acid Sequence↗
PubMed1987

In vitro immortalization of marmoset cells with three subgroups of herpesvirus saimiri.

Sequences within the rightmost 7 kilobases of the unique L DNA of herpesvirus saimiri are required for oncogenicity of the virus. The same DNA region has been found to be highly variable among different strains of herpesvirus saimiri. On the basis of this variability, herpesvirus saimiri strains were classified into groups A, B, and non-A, non-B. Herpesvirus saimiri strains representing the three groups were used successfully for in vitro immortalization of phytohemagglutinin-activated, interleukin 2 (IL-2)-expanded peripheral blood lymphocytes of common marmosets (Callithrix jacchus). Peripheral blood leukocytes could be immortalized from only a subset of common marmosets (5 of 13). All of the immortalized cell lines contained covalently closed circular viral DNA molecules and initially showed a low level of virus production. Cells immortalized by group A and group non-A, non-B strains did not require IL-2 in the medium. However, the only group B immortalized cell line, 473-SMHI, did not grow well in the absence of IL-2. The different characteristics of cell lines immortalized by herpesvirus saimiri strains belonging to different groups may help to elucidate some functions coded by the highly variable DNA region which is involved in the oncogenic process.

Animals↗
PubMed1992

Primary structure of the herpesvirus saimiri genome.

This report describes the complete nucleotide sequence of the genome of herpesvirus saimiri, the prototype of gammaherpesvirus subgroup 2 (rhadinoviruses). The unique low-G + C-content DNA region has 112,930 bp with an average base composition of 34.5% G + C and is flanked by about 35 noncoding high-G + C-content DNA repeats of 1,444 bp (70.8% G + C) in tandem orientation. We identified 76 major open reading frames and a set of seven U-RNA genes for a total of 83 potential genes. The genes are closely arranged, with only a few regions of sizable noncoding sequences. For 60 of the predicted proteins, homologous sequences are found in other herpesviruses. Genes conserved between herpesvirus saimiri and Epstein-Barr virus (gammaherpesvirus subgroup 1) show that their genomes are generally collinear, although conserved gene blocks are separated by unique genes that appear to determine the particular phenotype of these viruses. Several deduced protein sequences of herpesvirus saimiri without counterparts in most of the other sequenced herpesviruses exhibited significant homology with cellular proteins of known function. These include thymidylate synthase, dihydrofolate reductase, complement control proteins, the cell surface antigen CD59, cyclins, and G protein-coupled receptors. Searching for functional protein motifs revealed that the virus may encode a cytosine-specific methylase and a tyrosine-specific protein kinase. Several herpesvirus saimiri genes are potential candidates to cooperate with the gene for saimiri transformation-associated protein of subgroup A (STP-A) in T-lymphocyte growth stimulation.

Amino Acid Sequence↗
PubMedDate not supplied

Mechanisms of cell transformation by Herpesvirus saimiri.

Herpesvirus saimiri is a virus capable of inducing oncogenic transformation of T lymphocytes of New World primates and immortalizing human T cells in vitro. T lymphocytes immortalized by H. saimiri demonstrate functional biological responses to their antigens. Therefore, H saimiri-induced transformation of T cells emerges as a very powerful tool of T-cell biology. The mechanism of this transformation remains to be elucidated. However, it is apparent that H. saimiri proteins Tip and StpC are crucial for T-cell transformation. Potential mechanisms mediating the effects of Tip and StpC, as well as the possible role of other H. saimiri proteins, are discussed in this review.

CD2 Antigens↗
PubMedDate not supplied

Human T cells transduced by a retroviral vector to express Herpesvirus saimiri proteins TIP and STPC.

Herpesvirus saimiri is a virus capable of inducing oncogenic transformation of T lymphocytes of New World primates and immortalizing human T cells in vitro. T lymphocytes immortalized by H. saimiri demonstrate functional biological responses to their antigens. Therefore, H. saimiri-induced transformation of T cells emerges as a very powerful tool of T-cell biology. Although the mechanism of this transformation remains to be understood, it is thought that H. saimiri proteins Tip and StpC play important roles. To facilitate functional studies of Tip and StpC, we retrovirally transduced human MOLT4, Jurkat and JCaM1 T-cell lines to express these H. saimiri proteins, using a three-plasmid system allowing for rapid and efficient production of high-titer retroviral stocks. Several cell lines expressing Tip and/or StpC in a stable fashion were obtained and characterized.

3T3 Cells↗
PubMed1999

Haemobartonellosis in squirrel monkeys (Saimiri sciureus): antagonism between Haemobartonella sp. and experimental Plasmodium falciparum malaria.

A hemotropic parasite of the genus Haemo bartonella (rickettsial parasite of the Family Anaplasmataceae) is responsible for latent asymptomatic infection in colony-born Saimiri monkeys. Indeed, many of these animals develop a patent Haemobartonella infection following splenectomy. Such patent parasitism is characterized by an intense Haemobartonella parasitemia which peaks between days 12 and 14 after removal of the spleen and then decreases to become undetectable between days 25 and 30. During the resolving phase of parasitemia, a moderate anemia associated with monocytosis and erythrophagocytosis is observed. In certain Saimiri monkeys, Haemobartonella parasitemia remains latent following removal of the spleen. This indicates that the spleen plays a role but is not necessary to maintain latent Haemobartonella parasitism. It also suggests the existence of heterogeneity in the host immune reactivity to the parasite. Latent or patent haemobartonellosis might raise a problem when Saimiri monkeys are used as experimental hosts of Plasmodium falciparum asexual blood stages, as already noticed with "rodent malaria." Thus we investigated the relationship between Haemobartonella and P. falci parum in splenectomized monkeys. When animals harboring latent Haemobartonella sp. were infected with P. falciparum, the former remained latent and exerted no influence on the course of the P. falciparum parasitemia. In constrast, when P. falciparum was initiated in animals which were in the process of developing patent haemobarto nellosis, the course of the former was protracted and either the animal resisted longer, or it self-cleared the P. falciparum infection. Conversely, patent haemobartonellosis was delayed when splenectomy was performed at different times after initiation of P. falciparum infection in intact monkeys. Our results do not allow us to draw conclusions as to the mechanism(s) of the antagonism between the two parasites, but they emphasize the need to monitor the presence of Haemobartonella when splenectomized Saimiri monkeys are used as experimentals hosts for P. falciparum parasitism.

Anaplasmataceae Infections↗
PubMed1995

DNA evidence on the phylogenetic systematics of New World monkeys: support for the sister-grouping of Cebus and Saimiri from two unlinked nuclear genes.

Previous inferences from epsilon-globin gene sequences on cladistic relationships among the 16 extant genera of Ceboidea (the New World monkeys) were tested by strength of grouping and bootstrap values for the clades in the most parsimonious trees found: for this epsilon data set enlarged with additional Cebus and Saimiri orthologues; for another nuclear DNA sequence data set consisting of IRBP (interstitial retinol-binding protein gene) intron 1 orthologues; and for tandemly combined epsilon and IRBP sequences. Different ceboid species of the same genus always grouped strongly together as demonstrated by results on Cebus (capuchin monkeys), Saimiri (squirrel monkeys), Callicebus (titi monkeys), Aotus (night monkeys), Ateles (spider monkeys), and Alouatta (howler monkeys). Other strong groupings that could be represented as monophyletic taxa in a cladistic classification were: Cebuella (pygmy marmoset) and Callithrix (marmoset) into subtribe Callitrichina; Callitrichina, Callimico (Goeldi's monkey), Leontopithecus (lion tamarin), and Saguinus (tamarin) into subfamily Callitrichinae; Callitrichinae, Aotus, Cebus, and Saimiri into family Cebidae; Cacajao (uakari monkey) and Chiropotes (saki) into subtribe Chiropotina; Chiropotina and Pithecia (bearded saki) into tribe Pitheciini; Pitheciini and Callicebus into subfamily Pitheciinae; Brachyteles (woolly spider monkey), Lagothrix (woolly monkey), and Ateles into tribe Atelini; and Atelini and Alouatta into subfamily Atelinae. In addition the epsilon and IRBP results congruently grouped (but at lesser strengths) Brachyteles and Lagothrix into subtribe Brachytelina within Atelini, and also Cebus and Saimiri into subfamily Cebinae within Cebidae. Because the IRBP results weakly grouped Pitheciinae with Cebidae, whereas the epsilon results weakly grouped Pitheciinae with Atelinae, the present evidence is best represented in an interim cladistic classification of ceboids by dividing the superfamily Ceboidea into three families: Atelidae, Pitheciidae, and Cebidae.

Alouatta↗
PubMed1980

Onuf's nucleus of the sacral cord in a South American monkey (Saimiri): its location and bilateral cortical input from area 4.

A histological description of Onuf's nucleus, first described by Onuf as a sacral center for some striated muscles associated with the acts of erection and ejaculation in man, is reported in a South American monkey (Saimiri). Onuf's nucleus in Saimiri was organized into a well-defined cell group which consisted of medium-sized neurons with large and abundant Nissl bodies and was located in the ventrolateral aspect of the ventral horn of the first sacral segment of the spinal cord. Following horseradish peroxidase (HRP) injection into the external anal sphincter muscle in Saimiri, labeled neurons were found at the ipsilateral Onuf's nucleus. Additionally, a single injection of tritiated proline was made in the tail portion of area 4 of two Saimiri in order to study the cortical afferent connections of Onuf's nucleus. Autoradiographs revealed that corticospinal fibers might project directly to Onuf's nucleus. Onuf's nucleus, however, may be different in its cortical afferent connection compared with other somatic motor nuclei in the ventral horn of the cord. The termination is bilateral, i.e. some contralateral lateral corticospinal tract fibers apparently recross to end in the ipsilateral Onuf's nucleus.

Afferent Pathways↗
PubMedDate not supplied

Squirrel monkey (Saimiri sciureus) B lymphocytes: secretion of IgG directed to Plasmodium falciparum antigens, by primed blood B lymphocytes restimulated in vitro with parasitized red blood cells.

Blood B lymphocytes obtained from Plasmodium falciparum-immune Saimiri monkeys were assayed for their in vitro differentiation in immunoglobulin-secreting cells upon restimulation with P. falciparum-parasitized Saimiri red blood cells. Selected culture conditions enabled appropriately stimulated blood B cells to secrete 3F11/G10+ IgG, detected in the supernatants by means of a dot immunobinding assay. Primed blood B lymphocytes from P. falciparum-immune Saimiri monkeys were thus able to secrete IgG when restimulated by parasitized red blood cells in the presence of T cell- and monocyte-derived cytokines (recombinant human cytokines). These primed blood B cells, which were able to differentiate, were shown to secrete antibodies reactive with P. falciparum-infected red blood cells, as detected by means of an indirect immunofluorescence assay, and reactive with P. falciparum-infected red blood cell extracts, as detected by means of Western blot analysis. Furthermore, due to the possibility of discriminating between IgG subtypes in the squirrel monkey (3F11/G10+::3A2/G6+ IgG [associated with protection against the blood stages of P. falciparum] vs. 3F11/G10+::3E4/H8+ IgG [usually not functionally associated with protection]), we have attempted to estimate the respective proportions of each IgG subtype. In defined culture conditions, Saimiri monkey blood B cells preferentially secrete 3F11/G10+::3E4/H8+ IgG in response to parasitized red blood cells. We therefore discuss the conditions that would render this assay suitable for the selection, among P. falciparum blood stage antigens, of those that have major B-cell epitopes.

Animals↗