Disease relevance of Olfr6

• The regulation of two reporter genes, the essential viral M50 gene and a dominant-negative mutant gene (m48.2) encoding the small capsid protein, was analyzed in more detail [1].
• In mouse cytomegalovirus, a member of the betaherpesvirus subfamily, the homologous proteins M53/p38 and M50/p35 form the nuclear egress complex (NEC) [2].
• Protective effect of heterologous gram-positive vaccine against lethal upper respiratory tract infection with type M50 group A streptococci in mice [3].
• We inoculated 5 to 7-week-old female C3HeB/FeJ mice with Streptococcus pyogenes strain B514-Sm (type M50) by both an intranasal and intratracheal route and characterized the resulting illness [4].
• Significant resistance against M50 streptococci was also noted by i.n. application of heat-killed Lactobacillus fermenti (81% survival) as well as two strains of pneumococci (50 and 79% survival) [3].

High impact information on Olfr6

• We also used a fibroblastoid cell line (M50) and a monocytic tumor line (PU51R), which were not spontaneously killed [5].
• The collective results for many mutants localized the binding site for M50/p35 to amino acids (aa) 112 to 137 [2].
• Type M50 group A streptococci are exceptional for their virulence in mice [3].
• Treatment with the conjugate also resulted in an improvement in survival time of mice bearing ascitic M50 tumor, although the effects of a single dose of free drug, in the range of maximum tolerated doses, were marginal [6].
• The M50 type exhibited an LD100 a of 10(5) colony-forming units (CFU) when administered intranasally (i.n.), and of 10(7) CFU when introduced intraperitoneally (i.p.). I.n. administered vaccines prepared from M types 12, 18, 30, 49, 50 and 55 were equally efficient in preventing lethal infection after i.n. challenge with type M50 [7].

Analytical, diagnostic and therapeutic context of Olfr6

• Nor did vaccination with Escherichia coli and Pseudomonas aeruginosa induce protection against type M50 [3].

References