The drug monosodium luminol (GVT) preserves crypt-villus epithelial organization and allows survival of intestinal T cells in mice infected with the ts1 retrovirus

摘要: Abstract Of the cytopathic retroviruses that affect mammals, including HIV-1, many selectively infect CD4+ T cells and cause immunosuppressive syndromes. These diseases destroy both thymus small large intestines, after infecting killing T-lineage in tissues. A mutant of murine leukemia retrovirus MoMuLV-TB, called ts 1, causes this syndrome susceptible strains mice. In FVB/N strain mice are infected at birth, thymic atrophy, cell loss, intestinal collapse, body wasting, death occur by ∼30–40 days postinfection (dpi). Apoptosis 1-infected cells, thymus, peripheral lymphoid system intestines is caused accumulation 1 viral envelope preprotein gPr80 env , which inefficiently cleaved into mature proteins gp70 PrP15E. We show here infection intestine followed loss epithelial (IEC) thyroid-stimulating hormone (TSH) cycling gradients (along crypt-villus axes), apoptosis developing lamina propria (LP), collapse ∼30 dpi. treated with antioxidant drug monosodium luminol (GVT ® ), however, normal still place 30 dpi, IECs covering crypts villi contain amounts transcription factor Nrf2. addition, no apoptotic present, accumulated gpr80 absent from tissue time. conclude GVT treatment can make a noncytopathic virus for as it does thymocytes [25]. As may protect reducing oxidant stress perhaps prevention via Nrf2 upregulation IECs. results identify potential therapy or inflammatory conditions, HIV-AIDS, oxidative triggering exacerbating factor.