{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T01:09:26Z","timestamp":1782436166940,"version":"3.54.5"},"reference-count":40,"publisher":"Microbiology Society","issue":"12","license":[{"start":{"date-parts":[[2025,12,18]],"date-time":"2025-12-18T00:00:00Z","timestamp":1766016000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National University of Medical Sciences, Rawalpindi, Pakistan"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,12,18]]},"abstract":"<jats:p>\n                    <jats:bold>Introduction.<\/jats:bold>\n                    Host genetics plays a pivotal role in determining disease susceptibility among individuals infected with\n                    <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n                    . Scavenger receptors (SRs) such as\n                    <jats:italic>CD36<\/jats:italic>\n                    and\n                    <jats:italic>SR-B1<\/jats:italic>\n                    mediate pathogen recognition and lipid uptake, both of which are central to mycobacterial entry and immune modulation.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Gap Statement.<\/jats:bold>\n                    Polymorphisms rs1761667 and rs3211938 in\n                    <jats:italic>CD36<\/jats:italic>\n                    and rs4238001 in\n                    <jats:italic>SR-B1<\/jats:italic>\n                    have not been investigated in any population in relation to both latent tuberculosis infection (LTBI) and active tuberculosis (TB).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Aim.<\/jats:bold>\n                    To genotype\n                    <jats:italic>CD36<\/jats:italic>\n                    and\n                    <jats:italic>SR-B1<\/jats:italic>\n                    polymorphisms and evaluate their association with TB and LTBI. To predict the functional\/regulatory impact of these SNPs and compare their allele frequencies with global datasets.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methodology.<\/jats:bold>\n                    Polymorphisms were genotyped using amplification refractory mutation system PCR within a case-control design. Genotype frequencies were compared using Fisher\u2019s exact chi-square test. Functional and regulatory effects were predicted using PolyPhen-2 and RegulomeDB, while the 1000 Genomes database was used for population comparison.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results.<\/jats:bold>\n                    The homozygous AA genotype of\n                    <jats:italic>SR-B1<\/jats:italic>\n                    rs4238001 was strongly associated with active TB (\n                    <jats:italic>P<\/jats:italic>\n                    =0.00), while the heterozygous GA genotype showed a protective association with LTBI (\n                    <jats:italic>P<\/jats:italic>\n                    =0.00). For\n                    <jats:italic>CD36<\/jats:italic>\n                    , the homozygous GG genotype of rs3211938 was associated with protection against active TB (\n                    <jats:italic>P<\/jats:italic>\n                    =0.02) but exhibited the opposite pattern in LTBI (\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.00). Moreover, the heterozygous GA genotype of rs1761667 was significantly linked to increased risk of LTBI (\n                    <jats:italic>P<\/jats:italic>\n                    =0.00).\n                    <jats:italic>In silico<\/jats:italic>\n                    functional prediction classified rs4238001 as missense and rs3211938 as nonsense variant. Regulatory analysis indicated that rs4238001 and rs1761667 affect transcription in TB-relevant tissues. Population analysis highlighted variation in allele frequencies across groups.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion.<\/jats:bold>\n                    Polymorphisms in\n                    <jats:italic>SR-B1<\/jats:italic>\n                    and\n                    <jats:italic>CD36<\/jats:italic>\n                    show distinct associations with LTBI and TB, suggesting contrasting genetic influences on infection establishment and disease onset. These findings reveal a novel host genetic component of TB pathogenesis and warrant validation in larger, multiethnic cohorts.\n                  <\/jats:p>","DOI":"10.1099\/jmm.0.002111","type":"journal-article","created":{"date-parts":[[2025,12,18]],"date-time":"2025-12-18T12:17:16Z","timestamp":1766060236000},"source":"Crossref","is-referenced-by-count":1,"title":["CD36 and SR-B1 polymorphisms exhibit distinct association patterns in active and latent tuberculosis"],"prefix":"10.1099","volume":"74","author":[{"given":"Ezza Binte","family":"Tariq","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, National University of Medical Sciences, Rawalpindi, Pakistan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Urooj","family":"Subhan","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, The Women University, Multan, 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