Mass mortalities due to disease outbreaks have recently affected major taxa in the oceans. For closely monitored groups like corals and marine mammals, reports of the frequency of epidemics and the number of new diseases have increased recently. A dramatic global increase in the severity of coral bleaching in 1997—98 is coincident with high El Nino temperatures. Such climate-mediated, physiological stresses may compromise host resistance and increase frequency of opportunistic diseases. Where documented, new diseases typically have emerged through host or range shifts of known pathogens. Both climate and human activities may have also accelerated global transport of species, bringing together pathogens and previously unexposed host populations. T he oceans harbor enormous biodiver- sity by terrestrial terms (1), much of which is still poorly described taxo- nomically. Even less well known are the dy- namics of intermittent, ephemeral, threshold phenomena such as disease outbreaks. De- spite decades of intense study of the biolog- ical agents structuring natural communities, the ecological and evolutionary impact of diseases in the ocean remains unknown, even when these diseases affect economically and ecologically important species. The paucity of baseline and epidemiological information on normal disease levels in the ocean chal- lenges our ability to assess the novelty of a recent spate of disease outbreaks and to de- termine the relative importance of increased pathogen transmission versus decreased host resistance in facilitating the outbreaks. Our objectives here are to review the prevalence of diseases of marine taxa to evaluate wheth- er it can be concluded that there has been a recent increase. We also assess the contribut- ing roles of human activity and global cli- mate, and evaluate the role of the oceans as incubators and conveyors of human disease agents. Is There an Increase in Diseases in the Ocean?

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Emerging Marine Diseases--Climate Links and Anthropogenic Factors

This paper attempts to summarize current knowledge about immune responses to vaccines that correlate with protection. Although the immune system is redundant, almost all current vaccines work through antibodies in serum or on mucosa that block infection or bacteremia/viremia and thus provide a correlate of protection. The functional characteristics of antibodies, as well as quantity, are important. Antibody may be highly correlated with protection or synergistic with other functions. Immune memory is a critical correlate: effector memory for short-incubation diseases and central memory for long-incubation diseases. Cellular immunity acts to kill or suppress intracellular pathogens and may also synergize with antibody. For some vaccines, we have no true correlates, but only useful surrogates, for an unknown protective response.

Correlates of Protection Induced by Vaccination

The hope that hybridoma antibodies would reveal unique cell surface antigens during embryogenesis, differentiation and oncogenesis has been replaced by the realization that such antigens are mainly carbohydrate structures of glycoproteins and glycolipids occurring in many cell types. These findings either may reflect limitations in the methods of selection of hybridoma antibodies or may point to important roles for the diverse carbohydrate structures as receptors for regulators of cell growth and differentiation.

Demonstration by Monoclonal Antibodies That Carbohydrate Structures of Glycoproteins and Glycolipids Are Onco-Developmental Antigens

Measles virus continues to be a major killer of children, claiming roughly one million lives a year Measles virus infection causes profound immunosuppression, which makes measles patients susceptible to secondary infections accounting for high morbidity and mortality The Edmonston strain of measles virus, and vaccine strains derived from it, use as a cellular receptor human CD46 (refs 3, 4), which is expressed on all nucleated cells; however, most clinical isolates of measles virus cannot use CD46 as a receptor Here we show that human SLAM (signalling lymphocyte-activation molecule; also known as CDw150), a recently discovered membrane glycoprotein expressed on some T and B cells, is a cellular receptor for measles virus, including the Edmonston strain Transfection with a human SLAM complementary DNA enables non-susceptible cell lines to bind measles virus, support measles virus replication and develop cytopathic effects The distribution of SLAM on various cell lines is consistent with their susceptibility to clinical isolates of measles virus The identification of SLAM as a receptor for measles virus opens the way to a better understanding of the pathogenesis of measles virus infection, especially the immunosuppression induced by measles virus

SLAM (CDw150) is a cellular receptor for measles virus.

Multipotent mesenchymal stromal cells (MSCs) have unique immunoregulatory and regenerative properties that make them an attractive tool for the cellular treatment of autoimmunity and inflammation. Their underlying molecular mechanisms of action together with their clinical benefit - for example, in autoimmunity - are being revealed by an increasing number of clinical trials and preclinical studies of MSCs. However, autoimmunity and therapy-related alloimmunity are not only triggered and sustained by responses of the adaptive immune system; there is growing evidence that components of the innate immune system also have a key role. It is therefore important to study the crosstalk between MSCs and innate immunity, which ranges from the bone marrow niche to injured tissue.

Multipotent mesenchymal stromal cells and the innate immune system

Antigenic variation of human respiratory syncytial (RS) virus strains was analysed using a collection of nine, six, six, nine and one monoclonal antibodies respectively directed against the large glycoprotein (G), fusion protein (F), matrix protein (M), nucleoprotein (NP) and phosphoprotein (P) components of the Long strain of RS virus. A comparison was made with seven other strains isolated during different years in radioimmune precipitation analyses and immune fluorescence tests. Two different subtypes of the virus were demonstrable. Subtype A included the prototype strains Long and A2 and virus isolates from 1973, 1983 and 1984; subtype B included four virus strains isolated in successive years from 1979 to 1982. Subtype A viruses reacted with all the antibodies, whereas subtype B viruses showed different epitope characteristics in four structural components. The number of altered epitopes were 5/6, 1/2, 2/6 and 1/6 in the G, F, M and NP components, respectively. It is concluded that the two subtypes have evolved separately. The finding of two subtypes may explain previously observed strain variations in neutralization tests, and gives a new perspective on the immunobiology of RS virus.

Two distinct subtypes of human respiratory syncytial virus.

Specific pathogen free (SPF) domestic cats were inoculated with tissue homogenate obtained from a Chinese leopard (Panthera pardus japonensis) that had died in a North American zoo from a natural infection with canine distemper virus (CDV). The cats developed a transient cell-associated CDV viraemia along with pronounced lymphopenia but did not show any clinical symptoms. Plasma neutralizing-antibody titres against the homologous CDV (A92-27/4, isolated from the Chinese leopard) were consistently higher than against the CDV vaccine strain ‘Bussell’. The Chinese leopard CDV isolate showed in vitro biological properties reminiscent of virulent, wild-type CDV strains. Sequence analysis of the H gene of two large felid CDV isolates from the USA (A92-27/4 and A92-6) revealed up to 10% amino acid changes including up to four additional potential N-linked glycosylation sites in the extracytoplasmic domain as compared to CDV vaccine strains. Phylogenetic analysis was performed using the entire coding region of the H gene and a 388 bp fragment of the P gene of several morbillivirus species. Evidence was obtained that recent CDV isolates from different species in the United States (including isolates from large felids), Europe and Africa are significantly distinct from CDV vaccine strains. All wild-type CDV isolates analysed clustered according to geographical distribution rather than to host species origin. By sequence analysis a CDV epizootic among large felids in a Californian safari park was linked to a virus which most likely originated from feral non-felid carnivores.

Canine distemper virus from diseased large felids: Biological properties and phylogenetic relationships.

Measles virus phosphoprotein retains the nucleocapsid protein in the cytoplasm.

New series of escape mutants of human respiratory syncytial virus were prepared with monoclonal antibodies specific for the fusion (F) protein. Sequence changes selected in the escape mutants identified two new antigenic sites (V and VI) recognized by neutralizing antibodies and a group-specific site (I) in the F1 chain of the F molecule. The new epitopes, and previously identified antigenic sites, were incorporated into a refined prediction of secondary-structure motifs to generate a detailed antigenic map of the F glycoprotein.

Antigenic Structure of Human Respiratory Syncytial Virus Fusion Glycoprotein

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.

Claes Örvell

Papers

Two distinct subtypes of human respiratory syncytial virus.

Canine distemper virus from diseased large felids: Biological properties and phylogenetic relationships.

Measles virus phosphoprotein retains the nucleocapsid protein in the cytoplasm.

Antigenic Structure of Human Respiratory Syncytial Virus Fusion Glycoprotein

Respiratory syncytial virus epidemics: variable dominance of subgroups A and B strains among children, 1981-1986.