[Gerstmann-Sträussler-Scheinker syndrome].
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Animals↗
Biomedical subjects
Tetsutaro Sata
Publications and source records attributed to Tetsutaro Sata.
[Histopathological findings in cytomegalovirus retinitis].
PURPOSE: We examined eyeballs collected from autopsied acquired immunodeficiency syndrome patients with cytomegalovirus (CMV) retinitis, and analyzed the precise pathogenesis of CMV retinitis. MATERIAL AND METHODS: Eyeballs were fixed with 10% buffered formalin embedded in paraffin. CMV antigens were investigated by histopathological and immunohistochemical analyses. Histopathological findings were compared with funduscopic images. RESULTS: CMV antigens remained in the necrotic area of the retina and many CMV immediate early antigens existed in intact parts of the inner retina showing almost intact structure, and around retinal vessels. CONCLUSIONS: The results suggest that CMV infects the inner retina first via the retinal vessels, although funduscopic examination may appear normal. It extends through the neuronal cells and glial cells horizontally and Muller cells vertically. CMV severely damages the retinal structure.
AIDS-Related Opportunistic Infections↗
[Round table discussion on highly pathogenic H5N1 avian influenza].
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Animals↗
Transcriptional regulation of ILT family receptors.
Ig-like transcripts (ILT/leukocyte Ig-like receptor/monocyte/macrophage Ig-like receptor or CD85) are encoded on human chromosome 19q13.4, designated the human leukocyte receptor complex, and are predominantly expressed on myeloid lineage cells. We investigated the transcriptional regulation of ILT1, ILT2, and ILT4 genes to elucidate control mechanisms operating on the specific expression of ILT receptors. Inhibitory ILT2 and ILT4 both have a similar genomic structure, in which the approximately 160-bp 5'-flanking regions function as core promoters with critically important PU.1 binding sites. However, an Sp1 family-binding GC-box is more influential in trans-activation of ILT2 than ILT4. Additionally, ILT4 transcription is tightly regulated by chromatin modifications accompanied by histone acetylation, which strictly controls expression within myeloid lineage cells. Activating ILT1 carries a core promoter corresponding to the intronic region of ILT2 and ILT4, where PU.1 and Runx1 binding sites are essential, but a downstream heat shock element also augments promoter activity. Thus, each ILT is regulated by a distinct transcriptional mechanism, although PU.1 acts as a common trans-acting factor. We also found that human CMV infection strongly trans-activates inhibitory ILT2 and ILT4 genes through the expression of immediate-early proteins.
Antigens, CD↗
Protection against influenza virus infection by intranasal administration of C3d-fused hemagglutinin.
For the induction of mucosal immune responses by intranasal vaccination, cholera toxin B subunits (CTB) and Escherichia coli heat-labile toxin (LT) are often administered as mucosal adjuvants in order to enhance immune responses to mucosally co-administered bystander antigens. However, these toxin also are the causative agents of diarrhea. There is a demand for the establishment of an effective and safer adjuvant or vaccine that elicits mucosal immunity, but does not require the use of CTB or LT adjuvants. In order to induce protective mucosal immune responses in the nasal area against influenza virus infection, we have examined the recombinant protein composed of the complement component, C3d, which is fused to the secreted form of hemagglutinin (sHA-mC3d3) in the influenza-BALB/c mouse model. The fusion protein sHA-mC3d3, the secretory form of hemagglutinin, and the transmembrane form of HA (tmHA) from the influenza virus were intranasally administered to the mice with or without CTB containing a trace amount of holotoxin (CTB*) as an adjuvant. After intranasal administration of these proteins with CTB*, all mice produced nasal IgA and serum IgG antibodies (Abs) against the viral HA. In addition, viral infection was completely inhibited in these mice. In contrast, in the absence of the adjuvant, only sHA-mC3d3-induced locally secreted IgA and serum IgG Abs and provided complete protection against the influenza virus challenge. Thus, C3d fused to the influenza HA antigen is an effective and safe tool for mucosal vaccination.
Adjuvants, Immunologic↗
Human topoisomerase I promotes HIV-1 proviral DNA synthesis: implications for the species specificity and cellular tropism of HIV-1 infection.
Although HIV type 1 (HIV-1) cannot efficiently replicate in simian cells, the mechanism(s) involved in the restriction of virus tropism remain unclear. To investigate this, we have focused on the identification of human cellular factors that can influence the infectivity of HIV-1 derived from African green monkey producer cells. Whereas the infectivity of HIV-1 derived from such cells was only 10-15% of that of human cell-derived virus, expression of human topoisomerase I in the African green monkey cells resulted in a 5-fold increase of the infectivity of progeny HIV-1 virions. Replacement of glutamate-236 and asparagine-237 of human topoisomerase I with the corresponding residues (aspartate and serine, respectively) of the African green monkey enzyme abolished this enhancement of HIV-1 infectivity. This positive effect of human topoisomerase I expression in the African green monkey producer cells seemed to result from the promotion of HIV-1 cDNA synthesis. Thus, human topoisomerase I plays an important role in HIV-1 replication and infectivity, and differences in the species specificity of HIV-1 infection can at least in part be attributed to differences in topoisomerase I activities.
Amino Acid Sequence↗
Roles of anti-hemagglutinin IgA and IgG antibodies in different sites of the respiratory tract of vaccinated mice in preventing lethal influenza pneumonia.
The roles of IgA and IgG antibodies (Abs) against hemagglutinin (HA) in the prevention of lethal influenza pneumonia in vaccinated mice were examined in terms of distribution and concentration of the Abs in the mucus or the serous fluid in different sites of the respiratory tract (RT), mucosa of the nose, trachea, bronchi and bronchioli and the alveolar epithelia of pulmonary acinus. First, the surface areas of the tracheal, bronchial and bronchiolar mucosa and alveolar epithelia were measured to be 20, 260 and 217, 433 mm(2), respectively, using serial tissue sections of the trachea and lungs. Then, the volumes of the tracheal mucus, the bronchial and bronchiolar mucus and the serous fluid of alveolar epithelia were estimated to be 0.2, 2.6 and 21.7 mm(3), respectively, by calculating each from the surface area and an assumed thickness of the mucus layer (0.01 mm) or that of the serous fluid (0.0001 mm). Next, anti-HA IgA and IgG Ab responses in the nasal wash, the trachea-lung wash and the trachea wash were measured in BALB/c mice immunized intranasally with an adjuvant-combined A/PR/8/34 (H1N1) virus vaccine and challenged with a lethal dose of the virus. Then the values of Ab responses were converted to the mucus and serous fluid Ab concentration based on two premises that the serum Abs diffuse at a constant rate to the surface of the tracheal, bronchial and bronchiolar mucosa, and that the active transepithelial transport of IgA Abs does not work in the alveolar epithelia. Results showed that 21.4 microg/ml IgA Abs and 3.6 microg/ml IgG Abs in the tracheal mucus (19.1 and 0.3% of the trachea-lung wash IgA and IgG Ab amounts, respectively), 5.9 microg/ml IgA Abs and 3.6 microg/ml IgG Abs in the bronchial and bronchiolar mucus (66.0 and 3.4% of the trachea-lung wash IgA and IgG Ab amounts, respectively) and about 0.1 microg/ml IgA Abs and 12.3 microg/ml IgG Abs in the serous fluid of alveolar epithelia (14.9 and 96.3% of the trachea-lung wash IgA and IgG Ab amounts, respectively) were present in the vaccinated mice, at which concentrations influenza pneumonia was prevented. Thus, 96.3% of anti-HA IgG Abs in the trachea-lung wash work on the alveolar epithelia, whose surface area is about 800 times larger than that of tracheal, bronchial and bronchiolar mucosa and seem to play a more important role than the mucosal IgA Abs in the prevention of lethal influenza pneumonia.
Animals↗
Interleukin-8-mediated heterologous receptor internalization provides resistance to HIV-1 infectivity. Role of signal strength and receptor desensitization.
Human immunodeficiency virus type 1 (HIV-1) entry into CD4(+) cells requires the chemokine receptors CCR5 or CXCR4 as co-fusion receptors. We have previously demonstrated that chemokine receptors are capable of cross-regulating the functions of each other and, thus, affecting cellular responsiveness at the site of infection. To investigate the effects of chemokine receptor cross-regulation in HIV-1 infection, monocytes and MAGIC5 and rat basophilic leukemia (RBL-2H3) cell lines co-expressing the interleukin-8 (IL-8 or CXCL8) receptor CXCR1 and either CCR5 (ACCR5) or CXCR4 (ACXCR4) were generated. IL-8 activation of CXCR1, but not the IL-8 receptor CXCR2, cross-phosphorylated CCR5 and CXCR4 and cross-desensitized their responsiveness to RANTES (regulated on activation normal T cell expressed and secreted) (CCL5) and stromal derived factor (SDF-1 or CXCL12), respectively. CXCR1 activation internalized CCR5 but not CXCR4 despite cross-phosphorylation of both. IL-8 pretreatment also inhibited CCR5- but not CXCR4-mediated virus entry into MAGIC5 cells. A tail-deleted mutant of CXCR1, DeltaCXCR1, produced greater signals upon activation (Ca(2+) mobilization and phosphoinositide hydrolysis) and cross-internalized CXCR4, inhibiting HIV-1 entry. The protein kinase C inhibitor staurosporine prevented phosphorylation and internalization of the receptors by CXCR1 activation. Taken together, these results indicate that chemokine receptor-mediated HIV-1 cell infection is blocked by receptor internalization but not desensitization alone. Thus, activation of chemokine receptors unrelated to CCR5 and CXCR4 may play a cross-regulatory role in the infection and propagation of HIV-1. Since DeltaCXCR1, but not CXCR1, cross-internalized and cross-inhibited HIV-1 infection to CXCR4, the data indicate the importance of the signal strength of a receptor and, as a consequence, protein kinase C activation in the suppression of HIV-1 infection by cross-receptor-mediated internalization.
Acquired Immunodeficiency Syndrome↗
In situ hybridization AT-tailing with catalyzed signal amplification for sensitive and specific in situ detection of human immunodeficiency virus-1 mRNA in formalin-fixed and paraffin-embedded tissues.
In situ hybridization is one of the most important techniques to visualize gene expression at the cellular level in various tissues. The in situ hybridization-AT tailing (ISH-AT) method uses a specially designed and synthesized oligonucleotide probe that has (AT)10 on the 3' side. This (AT)10 of the probe is elongated by DeltaTth DNA polymerase in the presence of dATP, dTTP, and labeled dUTP in the tissue after hybridization. Through this process the target is labeled with many hapten molecules. In this study, we detected human immunodeficiency virus type 1 RNA in formalin-fixed and paraffin-embedded tissues obtained from autopsied patients with acquired immunodeficiency syndrome by combining ISH-AT with the catalyzed signal amplification (CSA) system (ISH-AT-CSA), although we failed to detect signals from the same samples by conventional in situ hybridization using RNA probes (RISH) with CSA (RISH-CSA). We demonstrated that the ISH-AT-CSA method was superior to RISH-CSA in terms of both sensitivity and specificity, and that it was applicable to fluorescence in situ hybridization and double staining with immunohistochemistry for the characterization of cell phenotypes.
Adenine↗
Simian TT virus (s-TTV) infection in patients with liver diseases.
Recently, we identified TTV isolates from nonhuman primates and named them simian TTV (s-TTV). To investigate the prevalence of s-TTV in humans, we examined sera from healthy individuals and patients with liver diseases in Japan for the presence of s-TTV DNA by PCR assay. s-TTV DNA was determined by nested PCR using s-TTV-specific primers designed from untranslated region of s-TTV genome. s-TTV DNA sequence was detected in three of 200 (1.5%) healthy adults but none of 48 infants without liver disease. On the other hand, s-TTV DNA was detected in 30 of 287 (10.5%) Japanese patients with liver disease. s-TTV coinfection with hepatitis B virus and hepatitis C virus were present in 16.7 and 30% of these patients, respectively, while 53.3% of patients were positive for s-TTV alone. Nucleotide sequence analyses in 20 patients confirmed that these PCR products were derived from s-TTV genome sequences and nearly 85% identical to those of s-TTV prototypes from chimpanzees. Phylogenetic analysis demonstrated that all s-TTV isolates from humans were distinguished clearly from the human TTV isolates. Furthermore, s-TTV in humans was classified into two different genotypes as well as simians. Our results indicate that generally 10.5% of Japanese patients with liver diseases were infected with s-TTV. The routes of s-TTV transmission from animal to human require clarification.
Journal Article↗
Prevalence of hepatitis virus types B through E and genotypic distribution of HBV and HCV in Ho Chi Minh City, Vietnam.
A molecular epidemiological survey of various hepatitis viral infections, including hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis D virus (HDV), was carried out in Ho Chi Minh City, Vietnam. This study included of 295 patients with liver disease (234 viral related and 61 non-viral related) and 100 healthy individuals. The infection rates of HBV and HCV in 234 liver disease patients with acute hepatitis, chronic hepatitis, liver cirrhosis and hepatocellular carcinoma, were 31.2 and 19.2%, respectively. On the other hand, detection rates of these viruses in healthy populations were 10 and 2%, respectively (P<0.005 and <0.0001, respectively). None of cases tested was positive for HDV RNA. The most common viral genotypes were type B and C of HBV (43 and 57%) and type 2a of HCV (33.3%). Surprisingly, high prevalence of HBV pre-S2 deletion mutant was found in 22 of 87 (25.3%) patients with chronic liver disease. Moreover, antibody to hepatitis E virus (HEV) immunoglobulin G (IgG) was detected in 78 of 185 (42%) and IgM in 1 of 185 (0.5%) patients. The age prevalence of anti-HEV IgG was reached 61.9% in 21-40-year-olds. These results suggest that these hepatitis viruses, except for HDV, are spreading among liver disease patients in Ho Chi Minh city, Vietnam and HBV was the most important causative agent correlated with liver disease in this area.
Journal Article↗
Latency-associated nuclear antigen of Kaposi's sarcoma-associated herpesvirus interacts with human myeloid cell nuclear differentiation antigen induced by interferon alpha.
Kaposi's sarcoma-associated herpesvirus (KSHV)/human herpes virus type 8 (HHV-8) is tightly linked to the development of Kaposi's sarcoma, primary effusion lymphoma (PEL) and some cases of multicentric Castleman's disease. Latency-associated nuclear antigen (LANA) is one of a limited number of KSHV genes consistently expressed in these diseases as well as in KSHV-infected cell lines derived from PEL, and has been shown to play crucial role in persistence of KSHV genomes in the infected cells. In this study, we explored the cellular factors that interact with LANA using yeast two-hybrid screening, and isolated a part of gene encoding human myeloid cell nuclear differentiation antigen (MNDA). MNDA is a hematopoietic interferon-inducible nuclear proteins with a HIN-200 family member with conserved 200-amino acid repeats. Immunoprecipitation assay revealed that LANA interacted with MNDA in a mammalian embryonic kidney cell line. MNDA transcript was undetectable in three PEL cell lines by reverse-transcription polymerase chain reaction, but it was induced by interferon alpha (IFNalpha). Moreover, LANA and MNDA were co-localized in the nuclei of MNDA-expressing PEL cells. Our results suggest that LANA interacts with MNDA in KSHV-infected cells exposed to IFNalpha. Such interaction may modulate IFN-mediated host defense activities.
Antigens, Differentiation, Myelomonocytic↗
High prevalence of hepatitis B virus pre-s mutant in countries where it is endemic and its relationship with genotype and chronicity.
It has been reported that hepatitis B virus (HBV) mutants carrying mutations in the pre-S region can be found in infected patients. In this study, we investigated the prevalence of the HBV variant with the pre-S mutant in different geographic regions, including countries with low and high levels of endemic HBV infection, and analyzed the correlation with clinical findings. We examined 387 HBV DNA-positive serum samples from individuals among 12 countries, consisting of Vietnam, Myanmar, Thailand, China, Korea, Nepal, Japan, Russia, Spain, United States, Bolivia, and Ghana. HBV pre-S mutants were detected in 71 (18.3%) of 387 serum samples tested. This mutant was the most prevalent in Vietnam (36%), followed by Nepal (27.3%), Myanmar (23.3%), China (22.4%), Korea (14.3%), Thailand (10.5%), Japan (7.7%), and Ghana (4.3%). In contrast, no case with this mutation was found in Russia, Spain, United States, and Bolivia. Among the HBV deletion mutations, 15.5% (11 of 71) occurred in the pre-S1 and 46.5% (33 of 71) in the pre-S2 regions. Eight (11.3%) cases had a mutation in both the pre-S1 and pre-S2 regions. In addition, a point mutation at the pre-S2 starting codon was observed in 19 (26.7%) cases. The detection rate of the HBV mutant in patients with hepatocellular carcinoma was significantly higher than in other patients (P < 0.05). Furthermore, these mutants were found more frequently in genotype B (25%) and genotype C (24.5%) than in the other genotypes (P < 0.05). Our results indicated that there was a high prevalence of HBV pre-S mutation in regions of endemic HBV infection in Asia. Furthermore, the pre-S mutation appeared to be correlated with hepatocellular carcinoma and HBV genotypes.
Amino Acid Sequence↗
Construction of an excisable bacterial artificial chromosome containing a full-length infectious clone of herpes simplex virus type 1: viruses reconstituted from the clone exhibit wild-type properties in vitro and in vivo.
In recent years, several laboratories have reported on the cloning of herpes simplex virus type 1 (HSV-1) genomes as bacterial artificial chromosomes (BACs) in Escherichia coli and on procedures to manipulate these genomes by using the bacterial recombination machinery. However, the HSV-BACs reported so far are either replication incompetent or infectious, with a deletion of one or more viral genes due to the BAC vector insertion. For use as a multipurpose clone in research on HSV-1, we attempted to generate infectious HSV-BACs containing the full genome of HSV-1 without any loss of viral genes. Our results were as follows. (i) E. coli (YEbac102) harboring the full-length HSV-1 genome (pYEbac102) in which a BAC flanked by loxP sites was inserted into the intergenic region between U(L)3 and U(L)4 was constructed. (ii) pYEbac102 was an infectious molecular clone, given that its transfection into rabbit skin cells resulted in production of infectious virus (YK304). (iii) The BAC vector sequence was almost perfectly excisable from the genome of the reconstituted virus YK304 by coinfection of Vero cells with YK304 and a recombinant adenovirus, AxCANCre, expressing Cre recombinase. (iv) As far as was examined, the reconstituted viruses from pYEbac102 could not be phenotypically differentiated from wild-type viruses in vitro and in vivo. Thus, the viruses grew as well in Vero cells as did the wild-type virus and exhibited wild-type virulence in mice on intracerebral inoculation. (v) The infectious molecular clone pYEbac102 is in fact useful for mutagenesis of the HSV-1 genome by bacterial genetics, and a recombinant virus carrying amino acid substitutions in both copies of the alpha0 gene was generated. pYEbac102 will have multiple applications to the rapid generation of genetically engineered HSV-1 recombinants in basic research into HSV-1 and in the development of HSV vectors in human therapy.
Alleles↗
Intravenous inoculation of replication-deficient recombinant vaccinia virus DIs expressing simian immunodeficiency virus gag controls highly pathogenic simian-human immunodeficiency virus in monkeys.
To be effective, a vaccine against human immunodeficiency virus type 1 (HIV-1) must induce virus-specific T-cell responses and it must be safe for use in humans. To address these issues, we developed a recombinant vaccinia virus DIs vaccine (rDIsSIVGag), which is nonreplicative in mammalian cells and expresses the full-length gag gene of simian immunodeficiency virus (SIV). Intravenous inoculation of 10(6) PFU of rDIsSIVGag in cynomologus macaques induced significant levels of gamma interferon (IFN-gamma) spot-forming cells (SFC) specific for SIV Gag. Antigen-specific lymphocyte proliferative responses were also induced and were temporally associated with the peak of IFN-gamma SFC activity in each macaque. In contrast, macaques immunized with a vector control (rDIsLacZ) showed no significant induction of antigen-specific immune responses. After challenge with a highly pathogenic simian-human immunodeficiency virus (SHIV), CD4(+) T lymphocytes were maintained in the peripheral blood and lymphoid tissues of the immunized macaques. The viral set point in plasma was also reduced in these animals, which may be related to the enhancement of virus-specific intracellular IFN-gamma(+) CD8(+) cell numbers and increased antibody titers after SHIV challenge. These results demonstrate that recombinant DIs has potential for use as an HIV/AIDS vaccine.
AIDS Vaccines↗
nef gene is required for robust productive infection by simian immunodeficiency virus of T-cell-rich paracortex in lymph nodes.
The pathogenesis of AIDS virus infection in a nonhuman primate AIDS model was studied by comparing plasma viral loads, CD4(+) T-cell subpopulations in peripheral blood mononuclear cells, and simian immunodeficiency virus (SIV) infection in lymph nodes for rhesus macaques infected with a pathogenic molecularly cloned SIVmac239 strain and those infected with its nef deletion mutant (Deltanef). In agreement with many reports, whereas SIVmac239 infection induced AIDS and depletion of memory CD4(+) T cells in 2 to 3 years postinfection (p.i.), Deltanef infection did not induce any manifestation associated with AIDS up to 6.5 years p.i. To explore the difference in SIV infection in lymphoid tissues, we biopsied lymph nodes at 2, 8, 72, and 82 weeks p.i. and analyzed them by pathological techniques. Maximal numbers of SIV-infected cells (SIV Gag(+), Env(+), and RNA(+)) were detected at 2 weeks p.i. in both the SIVmac239-infected animals and the Deltanef-infected animals. In the SIVmac239-infected animals, most of the infected cells were localized in the T-cell-rich paracortex, whereas in the Deltanef-infected animals, most were localized in B-cell-rich follicles and in the border region between the paracortex and the follicles. Analyses by double staining of CD68(+) macrophages and SIV Gag(+) cells and by double staining of CD3(+) T cells and SIV Env(+) cells revealed that SIV-infected cells were identified as CD4(+) T cells in either the SIVmac239 or the Deltanef infection. Whereas the many functions of Nef protein were reported from in vitro studies, our finding of SIVmac239 replication in the T-cell-rich paracortex in the lymph nodes supports the reported roles of Nef protein in T-cell activation and enhancement of viral infectivity. Furthermore, the abundance of SIVmac239 infection and the paucity of Deltanef infection in the T-cell-rich paracortex accounted for the differences in viral replication and pathogenicity between SIVmac239 and the Deltanef mutant. Thus, our in vivo study indicated that the nef gene enhances SIV replication by robust productive infection in memory CD4(+) T cells in the T-cell-rich region in lymphoid tissues.
Animals↗
Rapid tumor formation of human T-cell leukemia virus type 1-infected cell lines in novel NOD-SCID/gammac(null) mice: suppression by an inhibitor against NF-kappaB.
We established a novel experimental model for human T-cell leukemia virus type 1 (HTLV-1)-induced tumor using NOD-SCID/gammac(null) (NOG) mice. This model is very useful for investigating the mechanism of tumorigenesis and malignant cell growth of adult T-cell leukemia (ATL)/lymphoma, which still remains unclear. Nine HTLV-1-infected cell lines were inoculated subcutaneously in the postauricular region of NOG mice. As early as 2 to 3 weeks after inoculation, seven cell lines produced a visible tumor while two transformed cell lines failed to do so. Five of seven lines produced a progressively growing large tumor with leukemic infiltration of the cells in various organs that eventually killed the animals. Leukemic cell lines formed soft tumors, whereas some transformed cell lines developed into hemorrhagic hard tumors in NOG mice. One of the leukemic cell lines, ED-40515(-), was unable to produce visible tumors in NOD-SCID mice with a common gamma-chain after 2 weeks. In vivo NF-kappaB DNA binding activity of the ED-40515(-) cell line was higher and the NF-kappaB components were changed compared to cells in vitro. Bay 11-7082, a specific and effective NF-kappaB inhibitor, prevented tumor growth at the sites of the primary region and leukemic infiltration in various organs of NOG mice. This in vivo model of ATL could provide a novel system for use in clarifying the mechanism of growth of HTLV-1-infected cells as well as for the development of new drugs against ATL.
Animals↗
Prevalence of antibody against hepatitis E virus in various species of non-human primates: evidence of widespread infection in Japanese monkeys (Macaca fuscata).
We screened 495 serum samples from 20 species of non-human primates for the antibody against hepatitis E virus (HEV). Anti-HEV IgG was detected in 84 of 232 (36.2%) Japanese monkeys, 2 of 19 (10.5%) cynomolgus monkeys, 3 of 83 (3.6%) rhesus monkeys, and 1 of 1 (100%) Taiwanese monkey, respectively. These results suggest that HEV is circulating among monkeys belonging to the genus macaca. A high prevalence of anti-HEV IgG was observed in Japanese macaques (M. fuscata) despite the fact that Japan is non-endemic for hepatitis E. It is possible that HEV can be transmitted from Japanese macaques to humans. Further, the rate of antibody positivity was found to increase with age in Japanese macaques. Seropositive macaques were found throughout Japan, but the seroprevalence rate differed among geographic regions.
Animals↗