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The primary amino acid sequence within a stretch of 25 residues (positions 91–116) of the middle portion of the 3-′orf protein (p27 3′-orf) of the human immunodeficiency virus (HIV) shares structural homology with a highly charged region within the intracytoplasmic phosphorylation domain of human interleukin-2 receptor (IL-2R) and the ATP-binding site of the catalytic subunit of cAMP-dependent protein kinase (cAMP-PK) and other members of the protein kinase family. Comparison of the predicted secondary structure within this region of p27 3′-orf with the phosphorylation domain of human IL-2R and the ATP-binding region of the phospho-kinase family of protein suggests that the 3′-orf protein could serve homologous function(s).

Methyl groups placed on ϕXsB1 replicative form DNA by the Escherichia coliB modification enzyme are located in the overlap between fragments MboII-3 and AluI-2, a 61-base-pair DNA segment. Mutations that led to loss of susceptibility to restriction by E. coliB occurred within this segment at three positions spanning 14 nucleotides. A sequence difference between ϕXsB1 and ϕXam3cs70, a ϕX174 strain not restricted by E. coliB, occurs at one of these positions. The site on simian virus 40 DNA methylated by the modification enzyme is located in the 115-base-pair overlap between fragments HaeIII-I and AluI-G. The sequences of these segments of ϕXsB1 and simian virus 40 DNA and two regions of phage f1 DNA recognized by the E. coliB restriction enzyme [Ravetch, J. V., Horiuchi, K. & Zinder, N. D. (1978) Proc. Natl. Acad. Sci. USA75, 2266-2270] contain a homology of nine bases in the configuration:5′-T-G-A... 8N... T-G-C-T... 9N... T-N-N-T-3′.The sequence 5′-T-G-A... 8N... T-G-C-T-3′ may constitute the restriction enzyme recognition site since it does not occur in ϕXam3cs70 DNA and occurs only once in simian virus 40 DNA, and since all observed mutations leading to loss of the site occur at one of the bases specified by this sequence. Analysis of the sequence of ϕXam3cs70 showed that if no other residues are recognized, all seven of these bases are essential for recognition and the interval between the two groups of specified bases must be precisely eight.

T7 phage resists Escherichia coliB host-controlled modification and restriction in vivo, but its DNA carries roughly five sites which are susceptible to the purified enzymes.

The modification methylase of Escherichia coliB has been purified to apparent homogeneity. The enzyme can exist in several forms, each possessing two nonidentical polypeptides, β and γ, of molecular weights of 60,000 and 55,000, respectively. Freshly isolated enzyme has the structure β1γ1, but upon storage at neutral pH and low salt, it disproportionates, producing another form, β3γ1. Treatment at pH 5 converts the mixture of β3γ1and β1γ1to a mixture of β1γ1and another form β2γ1, whereas exposure to high salt breaks down the β3γ1structure. The enzyme is inhibited by S-adenosylethionine and 5′-methylthioadenosine, but not by S-adenosylhomocysteine. None of these compounds can replace the required cofactor, S-adenosylmethionine. The enzyme can methylate a wide variety of DNAs, but not DNA produced by E. coliB.

Objective: Mitochondrial function plays a role in both AIDS progression and HAART toxicity; therefore, we sought to determine whether mitochondrial DNA variation revealed novel AIDS restriction genes, particularly as mitochondrial DNA single-nucleotide polymorphisms are known to influence regulation of oxidative phosphorylation, reactive oxygen species production, and apoptosis.Design: This is a retrospective cohort study.Methods: We performed an association study of mitochondrial DNA haplogroups among 1833 European American HIV-1 patients from five US cohorts: the Multicenter AIDS Cohort Study, the San Francisco City Clinic Study, Hemophilia Growth and Development Study, the Multicenter Hemophilia Cohort Study, and the AIDS Linked to Intravenous Experiences cohort to determine whether the mitochondrial DNA haplogroup correlated with AIDS progression rate.Results: Mitochondrial DNA haplogroups J and U5a were elevated among HIV-1 infected people who display accelerated progression to AIDS and death. Haplogroups Uk, H3, and IWX appeared to be highly protective against AIDS progression.Conclusion: The associations found in our study appear to support a functional explanation by which mitochondrial DNA variation among haplogroups, influencing ATP production, reactive oxygen species generation, and apoptosis, is correlated to AIDS disease progression; however, repeating these results in cohorts with different ethnic backgrounds would be informative. These data suggest that mitochondrial genes are important indicators of AIDS disease progression in HIV-1 infected persons. [ABSTRACT FROM AUTHOR]