GI noroviruses are relatively rare and systematic studies of the molecular epidemiology of GI norovirus outbreaks are lacking. The current study examined the molecular virology of GI norovirus outbreaks in Victoria, Australia (2002-2010). Of 1,617 norovirus outbreaks identified, 69 (4.3%) were associated with GI norovirus alone, 1,540 (95.2%) with GII norovirus alone and 8 (0.5%) with GI + GII. Some differences between GI and GII outbreak epidemiology were found. GI outbreaks peaked in the 2-month period November/December whereas GII outbreaks peaked in the 2-month period September/October and GI norovirus outbreaks were significantly more common in non-healthcare settings (37.7%) than GII outbreaks (9.5%). ORF 1/ORF 2 genotypes found in the 69 outbreaks involving GI norovirus alone were: GI.2/GI.2, 7 outbreaks; GI.2/GI.6, 18 outbreaks; GI.3b/GI.3, 14 outbreaks; GI.4/GI.4, 21 outbreaks; GI.8/GI.8, one outbreak; GI.d/GI.3, four outbreaks; and GI.e/GI.13, one outbreak. The current study appears to be the first to have identified the recombinant form, GI.2/GI.6. Whereas GI.2/GI.6 and GI.3b/GI.3 outbreaks occurred with equal frequency in both healthcare and non-healthcare settings, GI.4/GI.4 occurred predominantly in healthcare settings. GI ORF 1/ORF 2 genotypes found in the eight outbreaks involving GI + GII norovirus were GI.2/GI.6, GI.3b/GI.3, and GI.4/GI.4, indicating GI genotypes in GI + GII outbreaks were similar to those found in outbreaks involving GI alone. Apparent differences in the evolution of different GI genotypes were noted. GI.2/GI.2, GI.2/GI.6, and GI.4/GI.4 strains tended to undergo periodic shifts in nucleotide sequence whereas various GI.3b/GI.3 strains tended to circulate simultaneously.

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Background: The Sydney blood bank cohort (SBBC) of long-term survivors consists of multiple individuals infected with attenuated, nef-deleted variants of human immunodeficiency virus type 1 (HIV-1) acquired from a single source. Long-term prospective studies have demonstrated that the SBBC now comprises slow progressors (SP) as well as long-term nonprogressors (LTNP). Convergent evolution of nef sequences in SBBC SP and LTNP indicates the in vivo pathogenicity of HIV-1 in SBBC members is dictated by factors other than nef. To better understand mechanisms underlying the pathogenicity of nef-deleted HIV-1, we examined the phenotype and env sequence diversity of sequentially isolated viruses (n = 2) from 3 SBBC members.

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