The Diversity and Biogeography of Western Indian Ocean Reef-Building Corals

This study assesses the biogeographic classification of the Western Indian Ocean (WIO) on the basis of the species diversity and distribution of reef-building corals. Twenty one locations were sampled between 2002 and 2011. Presence/absence of scleractinian corals was noted on SCUBA, with the aid of underwater digital photographs and reference publications for species identification. Sampling effort varied from 7 to 37 samples per location, with 15 to 45 minutes per dive allocated to species observations, depending on the logistics on each trip. Species presence/absence was analyzed using the Bray-Curtis similarity coefficient, followed by cluster analysis and multi-dimensional scaling. Total (asymptotic) species number per location was estimated using the Michaelis-Menten equation. Three hundred and sixty nine coral species were named with stable identifications and used for analysis. At the location level, estimated maximum species richness ranged from 297 (Nacala, Mozambique) to 174 (Farquhar, Seychelles). Locations in the northern Mozambique Channel had the highest diversity and similarity, forming a core region defined by its unique oceanography of variable meso-scale eddies that confer high connectivity within this region. A distinction between mainland and island fauna was not found; instead, diversity decreased radially from the northern Mozambique Channel. The Chagos archipelago was closely related to the northern Mozambique Channel region, and analysis of hard coral data in the IUCN Red List found Chagos to be more closely related to the WIO than to the Maldives, India and Sri Lanka. Diversity patterns were consistent with primary oceanographic drivers in the WIO, reflecting inflow of the South Equatorial Current, maintenance of high diversity in the northern Mozambique Channel, and export from this central region to the north and south, and to the Seychelles and Mascarene islands.     

Host plant utilization by butterfly larvae in the Andaman and Nicobar Islands (Indian Ocean)

The larval food plants of the butterflies of the Andaman and Nicobar islands have not been studied, although the butterfly fauna per se is fairly well known. For the first time we report the food plants of the larvae of 120 species of butterflies from these islands on the basis of laboratory rearing and field studies. This information is essential for the formulation of management programmes for butterfly conservation on these islands which are known to harbour critical swallowtail and (possibly) danaine faunas.     

Are the Indonesian and Western Indian Ocean Coelacanths Conspecific: A Prediction

It is hypothesized that the ancestor of the extant western Indian Ocean and Indonesian populations of Latimeria was continuously distributed along the deeper coasts of massed Africa–Madagascar–Eurasia in early geologic time. The collision of India with Eurasia, roughly 50 MY ago, caused the formation of the Himalayan Mountains and subsequent developement of numerous rivers. The rivers, which flow down both coasts of India, and areas even further east, deposited, and continue to deposit, great amounts of silt along both coasts of India. The siltation destroyed possible coelacanth habitats, thus isolating coelacanth populations to the west of India from those to the east and allowing them to diverge.     

Role of Host Immune Response and Viral Load in the Differential Outcome of Pandemic H1N1 (2009) Influenza Virus Infection in Indian Patients

Background

An unusually high number of severe pneumonia cases with considerable mortality is being observed with the pandemic H1N1 2009 virus infections globally. In India, all mild as well as critically ill cases were admitted and treated in the government hospitals during the initial phase of the pandemic. The present study was undertaken during this early phase of the pandemic.

Methodology

The role of viral load and host factors in the pathogenesis were assessed by examining 26 mild (MP), 15 critically ill patients (CIP) and 20 healthy controls from Pune, India. Sequential blood and lung aspirate samples were collected from CIP. Viral load and cytokines/chemokine levels were determined from the plasma and lung aspirates of the patients. TLR levels were determined by staining and FACS analysis. Gene profiling was done for both cells in the lung aspirates and PBMCs using TaqMan Low Density arrays. Antibody titres and isotyping was done using HA protein based ELISAs.

Principal Findings

13/15 critically ill patients expired. All plasma samples were negative for the virus irrespective of the patient''s category. Sequential lung samples from CIP showed lower viral loads questioning association of viral replication with the severity. Anti-rpH1N1-09-HA-IgG titres were significantly higher in critically ill patients and both categories circulated exclusively IgG1 isotype. Critically ill patients exhibited increase in TLR-3, 4, 7 and decrease in TLR-2 expressions. The disease severity correlated with increased plasma levels of IL1RA, IL2, IL6, CCL3, CCL4 and IL10. Majority of the immune-function genes were down-regulated in the PBMCs and up-regulated in the cells from lung aspirates of critically ill patients. No distinct pattern differentiating fatal and surviving patients was observed when sequential samples were examined for various parameters.

Conclusions

Disease severity was associated with pronounced impairment of host immune response.     

甲型流感病毒RNA聚合酶——抗病毒药物靶点

甲型流感病毒的RNA聚合酶由PB1、PB2和PA 三个亚基组成,在病毒的生命周期中负责行使病毒基因组的转录与复制等多方面功能. 甲型流感病毒由于频繁变异,导致其对传统抗病毒药物的敏感性降低,因此开发疗效好、针对性强、毒性低的新型抗病毒药物已成为当前亟待解决的问题.由于RNA聚合酶是甲型流感病毒生命周期重要的调控蛋白,并且编码聚合酶各亚基的基因序列具有高度保守性,故成为当前抗病毒药物的重要靶点.     

Increased Viral Loads and Exacerbated Innate Host Responses in Aged Macaques Infected with the 2009 Pandemic H1N1 Influenza A Virus

In contrast to seasonal influenza virus infections, which typically cause significant morbidity and mortality in the elderly, the 2009 H1N1 virus caused severe infection in young adults. This phenomenon was attributed to the presence of cross-protective antibodies acquired by older individuals during previous exposures to H1N1 viruses. However, this hypothesis could not be empirically tested. To address this question, we compared viral replication and the development of the immune response in naïve young adult and aged female rhesus macaques infected with A/California/04/2009 H1N1 (CA04) virus. We show higher viral loads in the bronchoalveolar lavage (BAL) fluid and nasal and ocular swabs in aged animals, suggesting increased viral replication in both the lower and upper respiratory tracts. T cell proliferation was higher in the BAL fluid but delayed and reduced in peripheral blood in aged animals. This delay in proliferation correlated with a reduced frequency of effector CD4 T cells in old animals. Aged animals also mobilized inflammatory cytokines to higher levels in the BAL fluid. Finally, we compared changes in gene expression using microarray analysis of BAL fluid samples. Our analyses revealed that the largest difference in host response between aged and young adult animals was detected at day 4 postinfection, with a significantly higher induction of genes associated with inflammation and the innate immune response in aged animals. Overall, our data suggest that, in the absence of preexisting antibodies, CA04 infection in aged macaques is associated with changes in innate and adaptive immune responses that were shown to correlate with increased disease severity in other respiratory disease models.     

Host Adaptation and the Alteration of Viral Properties of the First Influenza A/H1N1pdm09 Virus Isolated in Japan

A/Narita/1/2009 (A/N) was the first H1N1 virus from the 2009 pandemic (H1pdm) to be isolated in Japan. To better understand and predict the possible development of this virus strain, the effect of passaging A/N was investigated in Madin-Darby canine kidney cells, chicken eggs and mice. A/N that had been continuously passaged in cells, eggs, or mice obtained the ability to grow efficiently in each host. Moreover, A/N grown in mice had both a high level of pathogenicity in mice and an increased growth rate in cells and eggs. Changes in growth and pathogenicity were accompanied by amino acid substitutions in viral hemagglutinin (HA) and PB2. In addition, the adapted viruses exhibited a reduced ability to react with ferret antisera against A/N. In conclusion, prolonged passaging allowed influenza A/N to adapt to different hosts, as indicated by a high increase in proliferative capacity that was accompanied by an antigenic alteration leading to amino acid substitutions.     

Mixed Infection and the Genesis of Influenza Virus Diversity

The emergence of viral infections with potentially devastating consequences for human health is highly dependent on their underlying evolutionary dynamics. One likely scenario for an avian influenza virus, such as A/H5N1, to evolve to one capable of human-to-human transmission is through the acquisition of genetic material from the A/H1N1 or A/H3N2 subtypes already circulating in human populations. This would require that viruses of both subtypes coinfect the same cells, generating a mixed infection, and then reassort. Determining the nature and frequency of mixed infection with influenza virus is therefore central to understanding the emergence of pandemic, antigenic, and drug-resistant strains. To better understand the potential for such events, we explored patterns of intrahost genetic diversity in recently circulating strains of human influenza virus. By analyzing multiple viral genome sequences sampled from individual influenza patients we reveal a high level of mixed infection, including diverse lineages of the same influenza virus subtype, drug-resistant and -sensitive strains, those that are likely to differ in antigenicity, and even viruses of different influenza virus types (A and B). These results reveal that individuals can harbor influenza viruses that differ in major phenotypic properties, including those that are antigenically distinct and those that differ in their sensitivity to antiviral agents.Influenza viruses (family Orthomyxoviridae) possess a negative-strand segmented RNA genome and enveloped virions. Genetic diversity in influenza virus is the result of a high rate of mutation associated with replication using low-fidelity RNA polymerase and of the reshuffling (or reassortment) of segments among coinfecting strains. Although the 13.5-kb genome of influenza A virus is composed of eight segments coding for 11 known proteins, these viruses are typically categorized by their two surface antigens, hemagglutinin (HA), of which there are 16 subtypes (H1 to H16), and neuraminidase (NA), of which there are 9 (N1 to N9) (9). All known subtypes are present in aquatic birds of the orders Anseriformes and Charadriformes, and a smaller number circulate in some mammalian species. The HA plays a major role in the attachment of the virus to the host cell surface by binding to the sialic acid moiety of host receptors and facilitating the fusion of the viral envelope with host cell membranes. It is also the major viral antigen against which neutralizing antibodies are directed. The NA is important for mobility of the virions by cleaving the sialic acid residues from the viral hemagglutinin, which facilitates both entry of the virus into the cell and release of the viruses during budding (11).Most discussions of influenza virus evolution have focused on the process of antigenic drift in which mutations accumulate—most likely by natural selection—in the antigenic sites of the HA and NA, thereby allowing evasion of the host populations’ acquired immunity to previously circulating strains. Such antigenic variation occurs primarily in the HA1 domain and is clustered into five main epitope regions (19, 20, 22). Although antigenic drift clearly plays a key role in the seasonal evolution of influenza A virus, recent studies making use of large data sets generated by the Influenza Genome Sequencing Project (IGSP) suggest that reassortment may also be important in the generation of antigenically novel isolates by placing diverse HAs in compatible genetic backgrounds (6, 8, 10, 14).Segment reassortment is also central to the process of cross-species transmission and emergence of pandemic influenza virus. In particular, the segmented nature of the influenza virus genome allows reassortment of gene segments to occur between diverse influenza A virus strains when they coinfect a single host, including those derived from different species. This can result in subtle changes within a subtype, or dramatic changes that occur when different subtypes mix, leading to the generation of novel viruses expressing surface glycoproteins to which a specific host immune system has little if any serological cross-reactivity. Such antigenic shift is believed to have led to the emergence of global human influenza A virus pandemics in 1957 (A/H2N2) and in 1968 (A/H3N2), with new segments ultimately derived from the avian reservoir pool reassorting into human influenza viruses (17).Given the potential for emerging viruses such as influenza virus to adversely affect the health of human and other animal populations, it is essential to determine the factors that allow viruses to acquire the mutations they need to adapt to new host populations. As a large number of point mutations are thought to be required for an avian influenza virus such as A/H5N1 to evolve sustained transmission in human populations (5), one likely scenario for successful emergence is through the acquisition of genetic material from a viral subtype already adapted to humans, such as A/H1N1 or A/H3N2. This would require that viruses of both subtypes coinfect the same cells, thereby generating a mixed infection, and then exchange genomic segments through reassortment, as was the case in 1957 and 1968. As a consequence, it is crucial to determine the frequency with which mixed infection naturally occurs in influenza A virus as well as its phenotypic consequences. To address these questions we undertook, for the first time, in-depth sequencing of multiple viral genome sequences sampled from individual influenza patients. These studies were performed with approval of the New York State (study numbers 04-103 and 02-054) and University of Pittsburgh (08-110400) institutional review boards.     

宿主miRNA参与甲型流感病毒复制调控研究进展

流行性感冒（简称“流感”）是由流感病毒引起的急性呼吸道传染疾病,据世界卫生组织统计,流感每年可导致300万～500万严重病例,其中29万～65万病例死亡,给社会带来沉重的经济负担,是一个世界性的公共卫生难题。研究发现宿主细胞中存在多条信号通路参与对流感病毒感染的应答,越来越多的研究表明宿主miRNAs通过直接或间接的方式,在流感病毒感染、复制的不同阶段发挥着重要调控作用。本文综合分析了目前关于宿主细胞miRNA对流感病毒复制调控的研究进展,对不同的miRNA具体的调控机制进行系统地归类总结后发现：甲型流感病毒（Influenza A virus,IAV）的PB1、PB2、NA、NP、M1基因是宿主miRNA直接抑制病毒复制的主要靶基因,而在间接调控过程中宿主miRNA主要作用在RIG-I样受体信号通路,Jak-STAT信号通路和Toll样受体信号通路三条流感病毒应答信号途径中,以上发现将更有助于全面理解宿主miRNA对于流感病毒调控网络和宿主细胞与流感病毒的互作机制。     

Influenza Virus in a Natural Host,the Mallard: Experimental Infection Data

Wild waterfowl, particularly dabbling ducks such as mallards (Anas platyrhynchos), are considered the main reservoir of low-pathogenic avian influenza viruses (LPAIVs). They carry viruses that may evolve and become highly pathogenic for poultry or zoonotic. Understanding the ecology of LPAIVs in these natural hosts is therefore essential. We assessed the clinical response, viral shedding and antibody production of juvenile mallards after intra-esophageal inoculation of two LPAIV subtypes previously isolated from wild congeners. Six ducks, equipped with data loggers that continually monitored body temperature, heart rate and activity, were successively inoculated with an H7N7 LPAI isolate (day 0), the same H7N7 isolate again (day 21) and an H5N2 LPAI isolate (day 35). After the first H7N7 inoculation, the ducks remained alert with no modification of heart rate or activity. However, body temperature transiently increased in four individuals, suggesting that LPAIV strains may have minor clinical effects on their natural hosts. The excretion patterns observed after both re-inoculations differed strongly from those observed after the primary H7N7 inoculation, suggesting that not only homosubtypic but also heterosubtypic immunity exist. Our study suggests that LPAI infection has minor clinically measurable effects on mallards and that mallard ducks are able to mount immunological responses protective against heterologous infections. Because the transmission dynamics of LPAIVs in wild populations is greatly influenced by individual susceptibility and herd immunity, these findings are of high importance. Our study also shows the relevance of using telemetry to monitor disease in animals.     

Haemoproteus iwa in Great Frigatebirds (Fregata minor) in the Islands of the Western Indian Ocean

Blood parasites of the sub-genus Haemoproteus have been reported in seabirds, in particular in species in the Suliformes order. These parasites are transmitted by hippoboscid flies of the genus Olfersia; strong specificity has been suggested between the vector and its vertebrate host. We investigated the prevalence of Haemoproteus infection in Suliformes and hippoboscid flies in two oceanic islands of the Western Indian Ocean: Europa and Tromelin. In total, 209 blood samples were collected from great frigatebirds (Fregata minor), masked boobies (Sula dactylatra) and red-footed boobies (Sula sula). Forty-one hippoboscid flies were also collected from birds. Seventeen frigatebirds and one fly collected on Europa tested positive for the presence of Haemoproteus parasites by polymerase chain reaction. Phylogenetic analyses based on partial sequences of the Cytochrome b gene showed that parasites were closely related to Haemoproteus iwa reported from frigatebirds in the Pacific Ocean and in the Caribbean. Plasmodium was also detected in a frigatebird on Europa; however, its placement on the phylogenetic tree could not be resolved. We provide strong support for transmission of blood parasites in seabirds in the Western Indian Ocean and suggest that migrations between the Pacific and the Indian oceans could favor the large-scale distribution of Haemoproteus iwa in frigatebird populations.     

Influenza A: Understanding the Viral Life Cycle

Influenza A virus belongs to the family of Orthomyxoviridae. It is an enveloped virus with a negative sense RNA segmented genome that encodes for 11 viral genes. This virus has evolved a number of mechanisms that enable it to invade host cells and subvert the host cell machinery for its own purpose, that is, for the sole production of more virus. Two of the mechanisms that the virus uses are “cap-snatching” and preventing the host cell from expressing its own genes. This mini-review provides a brief overview as to how the virus is able to invade host cells, replicate itself, and exit the host cell.