No abstract

Bacterial community composition and functional potential change subtly across gradients in the surface ocean. In contrast, while there are significant phylogenetic divergences between communities from freshwater and marine habitats, the underlying mechanisms to this phylogenetic structuring yet remain unknown. We hypothesized that the functional potential of natural bacterial communities is linked to this striking divide between microbiomes. To test this hypothesis, metagenomic sequencing of microbial communities along a 1,800 km transect in the Baltic Sea area, encompassing a continuous natural salinity gradient from limnic to fully marine conditions, was explored. Multivariate statistical analyses showed that salinity is the main determinant of dramatic changes in microbial community composition, but also of large scale changes in core metabolic functions of bacteria. Strikingly, genetically and metabolically different pathways for key metabolic processes, such as respiration, biosynthesis of quinones and isoprenoids, glycolysis and osmolyte transport, were differentially abundant at high and low salinities. These shifts in functional capacities were observed at multiple taxonomic levels and within dominant bacterial phyla, while bacteria, such as SAR11, were able to adapt to the entire salinity gradient. We propose that the large differences in central metabolism required at high and low salinities dictate the striking divide between freshwater and marine microbiomes, and that the ability to inhabit different salinity regimes evolved early during bacterial phylogenetic differentiation. These findings significantly advance our understanding of microbial distributions and stress the need to incorporate salinity in future climate change models that predict increased levels of precipitation and a reduction in salinity.

A panel of 20 recombinant Fab fragments reactive with the surface glycoprotein gpl20 of human type 1 immunodeficiency virus (HIV-1) were examined for their ability to neutralize MN and hUB strains of the virus. Neutralization was determined as the ability of the Fab fragments to inhibit infection as measured in both a p24 ELISA and a syncytium-formation assay. One group of closely sequencerelated Fab fragments was found to neutralize virus in both assays with a 50% neutralization titer at -1 ,ug/ml. AnotherFab neutralized in the p24 ELISA but not in the syncytium assay. The other Fab fragments showed weak or no neutralizing ability. The results imply that virion aggregation or crosslinking of gp120 molecules on the virion surface is not an absolute requirement for HIV-1 neutralization. Further, all of the Fab fragments were shown to be competitive with soluble CD4 for binding to gpl20 and yet few neutralized the virus effectively, implying that the mechanism of neutralization in this case may not involve receptor blocking. The observation of a preponderance ofhigh-affminty Fab fragments with poor or no neutralizing ability could have implications for vaccine strategies.

SUMMARYA radioimmunoprecipitation assay (RIPA) was used to study the serum antibody responses to individual polypeptides that developed after infection with viruses from human rotavirus subgroups I and II. Paired sera from eight children (1 to 8.5 years of age) were used in the study. Although all of the eight acute sera were negative by the complement fixation test, four of them were positive by RIPA, indicating a previous infection by rotavirus. A significant difference in the number of polypeptides immunoprecipitated was seen among the convalescent sera. The number of polypeptides immunoprecipitated was found to be related to previous infection experience. At most, ten different polypeptides were immunoprecipitated: seven structural polypeptides VPl to VP7 and three non-structural polypeptides, NSl, NS 2 and NS3. No sera immunoprecipitated VP8 or VP9. Acute sera positive by RIPA immunoprecipitated up to five polypeptides, VP1, VP2, VP3, VP4 and VP6. One of the non-structural proteins (NS2) was found to be particularly immunogenic, since antibodies to this polypeptide were detected in several convalescent sera. Among the structural proteins VP2 and VP6 were found to be the two immunodominant polypeptides which were recognized by all convalescent sera. Only three convalescent sera immunoprecipitated VP7, the major type-specific antigen responsible for inducing neutralizing antibodies. Three of four originally seronegative children with no reactivity in the convalescent sera to VP7 developed neutralizing antibodies to a single serotype. One child developed antibodies to two serotypes.

SUMMARYThe structural polypeptides of two strains of measles virus grown in Vero cells were analysed in SDS-PAGE slab gels. Six major polypeptides were identified with mol. wt. of 79o00, 72ooo, 6oooo, 430o0, 4oooo and 36ooo. The largest polypeptide was sensitive to trypsin digestion and was the dominant glycosylated polypeptide identified when the virus was grown in medium containing 3H-fucose or ZH-glucosamine or when the virus was treated with galactose oxidase and labelled with 3H-sodium borohydride. It is concluded that the 79 ooo mol. wt. polypeptide represents the haemagglutinin. Treatment with non-ionic detergent removed this polypeptide and also the 40oo0 tool. wt. polypeptide from the virus envelope. The 4oooo tool. wt. polypeptide is probably associated with haemolysin and cell fusion activities and is analogous to the F1 of paramyxoviruses. A polypeptide of tool. wt. approx. 2oooo detected after glycoprotein labelling may represent the F2 of measles virus. The 430o0 mol. wt. polypeptide co-migrates with cellular actin and is the only major measles polypeptide that is heavily labelled when the virus is grown on Veto cells prelabelled with 35S-methionine. Thus it may represent cellular actin incorporated into the virus during maturation. The quantity of the 72oo0 mol. wt. polypeptide relative to the other major polypeptides varied considerably in different virus preparations. The role of the polypeptide could not be defined. By analogy with previously published data the 6oooo and 36o00 tool. wt. polypeptides are inferred to represent nucleocapsid and membrane proteins, respectively.

It is proposed that the family Paramyxoviridae shall comprise three genera: Paramyxovirus, Morbillivirus, and Pneumovirus.

We examined the distribution of subgroups A and B strains from respiratory syncytial virus during five epidemic years from 1981 to 1986 in Huntington, West Virginia. Of 235 infants and children with respiratory syncytial virus infection, 211 had virus reisolated from frozen throat swab specimens for subgroup characterization by reactivity with a panel of monoclonal antibodies to the G, F, NP, M, and P proteins by using an enzyme immunoassay. We identified 160 (75.8%) strains as subgroup A and 51 (24.2%) as subgroup B. Strains of both subgroups were isolated in all years. Small, but approximately equal, numbers of subgroup B strains were isolated each epidemic year. By contrast, subgroup A strains occurred at least three times as often in all years except 1984-1985. The very low number of subgroup A strains isolated during the 1984-1985 epidemic gave dominance to subgroup B strains.

Infection of macaques with simian immunodeficiency virus (SIV) and human immunodeficiency virus type 2 (HIV-2) are useful models for studies of immunotherapy and vaccination against HIV as well as for testing of antiviral drugs. Vaccine research showing protective immunity in immunized monkeys has indicated that it will be possible to develop a vaccine for prevention of human HIV infection, although many hurdles remain. The design of an HIV vaccine would be helped if the basis of the protective immunity could be elucidated. Passive immune prophylaxis offers a means to determine the relative role of antibodies in protection against infection. We have studied whether a transfer of antibodies can prevent HIV-2 and SIVsm (SIV of sooty mangabey origin) infection in cynomolgus monkeys. Sera with high antibody titres were collected, heat-treated and injected into naive animals 6 h before challenge with 10-100 monkey-infectious doses of live homologous virus. All control animals treated with normal monkey serum (n = 6) or no serum (n = 39) became infected by the challenge virus, whereas five out of seven animals pretreated with antibody-containing serum at a dose of 9 ml kg-1 resisted infection. Thus passively transferred antibodies can protect against a low-dose lentivirus challenge in a nonhuman primate.