Transfusion-transmitted HTLV-I and -II are similar. The data suggest that a donor's lymphocytes become noninfectious when they lose the ability to be activated or to proliferate.

The DNA genomes of human T-lymphotropic virus type III (HTLV-III) isolated from 18 individuals with AIDS or who were at risk for AIDS were evaluated for evidence of variation. Although all of the 18 viral DNA's hybridized throughout their entire genomes to a full-length cloned probe of the original HTLV-III isolate, each of the 18 isolates showed a different restriction enzyme pattern. The number of restriction site differences between isolates ranged from only 1 site in 23 to at least 16 sites in 31. No particular viral genotype was associated with a particular disease state and 2 of the 18 patients had evidence of concurrent infection by more than one viral genotype. Propagation of three different viral isolates in vitro for up to 9 months did not lead to detectable changes in their restriction patterns. These findings indicate that different isolates of HTLV-III comprise a spectrum of highly related but distinguishable viruses and have important implications regarding the pathogenicity of HTLV-III and attempts to develop effective diagnostic, therapeutic, and preventive measures for this virus.

Objective To investigate the distribution of known factors for preterm birth (PTB) by severity of maternal underweight; to investigate the risk adjusted relationship between severity of underweight and PTB and to assess if the relationship differed by gestational age. Design Retrospective cohort study. Setting State of California, USA. Methods Maternally linked hospital and birth certificate records of 950,356 California deliveries in 2007–2010 were analyzed. Singleton live births of women whose pre-pregnancy body mass index (BMI) was underweight (<18.5 kg/m2) or normal (18.50–24.99 kg/m2) were analyzed. Underweight BMI was further categorized as: severe (<16.00), moderate (16.00–16.99) or mild (17.00–18.49). PTB was grouped as 22–27, 28–31, 32–36 or <37 weeks (compared with 37–41 weeks). Adjusted multivariable Poisson regression modeling was used to estimate relative risk for PTB. Main outcome measures Risk of PTB. Results 72,686 (7.6%) women were underweight. Increasing severity of underweight was associated with increasing percent PTB: 7.8% (n=4421) in mild, 9.0% (n=1001) in moderate and 10.2% (475) in severe underweight. The adjusted relative risk of PTB also significantly increased: aRR=1.22 (95%CI: 1.19–1.26) in mild, aRR=1.41 (95%CI: 1.32–1.50) in moderate and aRR=1.61 (95%CI: 1.47–1.76) in severe underweight. These findings were similar in spontaneous PTB, medically indicated PTB, and the gestational age groupings. Conclusion Increasing severity of maternal pre-pregnancy underweight BMI was associated with increasing risk adjusted PTB at <37 weeks. This increasing risk was of similar magnitude in spontaneous and medically indicated births and in preterm delivery at 28–31 and at 32–36 weeks of gestation.

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A recombinant protein of the human T cell lymphotropic virus type I (HTLV-I) gp46 outer membrane envelope, MTA-4 (residues 129-203), reacted by Western blot with sera from HTLV-I-infected individuals from the United States and Jamaica but not with 24 (10%) of 242 Japanese sera. A related gp46 recombinant protein, MTA-1 (residues 162-209), reacted with all 58 sera from HTLV-I-infected US and Jamaican individuals and 238 of 242 sera from infected Japanese (combined sensitivity of 99%). Neither recombinant showed reactivity to sera from HTLV-II-infected individuals or uninfected controls. The reactivity of recombinant proteins containing the region of HTLV-II gp46 analogous to MTA-1 was also evaluated by Western blot: GH2-K15 (residues 157-205) and GH2-K55 (residues 162-205) reacted with 88 (98%) and 89 (99%), respectively, of 90 sera from HTLV-II-infected individuals but not with sera from HTLV-I-infected individuals or uninfected controls. These recombinant proteins should permit the development of assays to unambiguously confirm and differentiate HTLV-I and HTLV-II infections.