Whitefly resistance traits derived from the wild tomato Solanum pimpinellifolium affect the preference and feeding behavior of Bemisia tabaci and reduce the spread of Tomato yellow leaf curl virus.

Breeding of tomato genotypes that limit whitefly (Bemisia tabaci) access and feeding might reduce the spread of Tomato yellow leaf curl virus (TYLCV), a begomovirus (genus Begomovirus, family Geminiviridae) that is the causal agent of tomato yellow leaf curl disease. TYLCV is restricted to the phloem and is transmitted in a persistent manner by B. tabaci. The tomato breeding line ABL 14-8 was developed by introgressing type IV leaf glandular trichomes and secretion of acylsucroses from the wild tomato Solanum pimpinellifolium accession TO-937 into the genetic background of the whitefly- and virus-susceptible tomato cultivar Moneymaker. Results of preference bioassays with ABL 14-8 versus Moneymaker indicated that presence of type IV glandular trichomes and the production of acylsucrose deterred the landing and settling of B. tabaci on ABL 14-8. Moreover, electrical penetration graph studies indicated that B. tabaci adults spent more time in nonprobing activities and showed a reduced ability to start probing. Such behavior resulted in a reduced ability to reach the phloem. The superficial type of resistance observed in ABL 14-8 against B. tabaci probing significantly reduced primary and secondary spread of TYLCV.

Multiple Resistance to Meloidogyne spp. and to Bipartite and Monopartite Begomovirus spp. in Wild Solanum (Lycopersicon) Accessions.

The Ty-1 locus confers tolerance to monopartite and bipartite Begomovirus spp. (genus Begomovirus, family Geminiviridae) and this phenotype is improved in homozygous tomato lines. However, the gene Mi (Meloidogyne spp. resistance) is in repulsion phase linkage with Ty-1, which hampers the large-scale development of multiresistant inbred lines. Seventy-one Solanum (section Lycopersicon) accessions were whitefly inoculated with the bipartite Begomovirus sp. Tomato rugose mosaic virus (ToRMV) and simultaneously infested with a mixture of Meloidogyne incognita and M. javanica under greenhouse conditions in Brazil. Accessions were then transplanted into a nematode-infested field with natural ToRMV infection. A severity index was used to evaluate ToRMV reaction. Nematode evaluation was done by counting the number of galls per root system. Seventeen accessions with Meloidogyne spp. and ToRMV resistance were selected and evaluated in Spain against three monopartite Begomovirus spp. associated with the tomato yellow leaf curl virus disease, using infectious clones. Systemic infection was monitored by DNA hybridization. Five S. peruvianum accessions (PI-306811, PI-365951, LA-1609, LA-2553, and CNPH-1194) displayed nematode and broad-spectrum resistance to all Begomovirus spp. tested in both continents. From the breeding standpoint, accessions combining resistance to Meloidogyne spp. and to bipartite and monopartite Begomovirus spp. would be useful for the development of elite lines expressing all traits in homozygous condition.

Phenotypic expression, stability, and inheritance of a recessive resistance to monopartite begomoviruses associated with tomato yellow leaf curl disease in tomato.

Tomato-infecting begomoviruses comprise a complex of monopartite and bipartite virus species that cause severe yield and quality losses worldwide. Therefore, the availability of wide spectrum resistance for begomovirus control is desirable. However, limited sources of resistance are available. In this study, three tomato inbred lines with resistance to bipartite begomoviruses of Brazil were tested for resistance to monopartite begomoviruses associated with the tomato yellow leaf curl disease (TYLCD). Stable resistance to Tomato yellow leaf curl virus was observed either by inoculation with Bemisia tabaci or with Agrobacterium tumefaciens using an infectious clone. The resistance resulted in a complete absence of TYLCD symptoms and restricted virus accumulation. Further studies performed with the line '468-1-1-12' indicated that the resistance was also effective against three other virus species associated with TYLCD, indicating wide spectrum resistance of this source. Quantitative genetics analyses suggested that a major recessive locus with epistatic interactions is controlling the resistance to TYLCD in '468-1-1-12', which could facilitate introgression of this trait into elite tomato lines. The resistance was stable under field conditions with high TYLCD pressure. Mild symptoms could be observed in these conditions, and recovery from disease and from virus infection suggested an active host antiviral defense mechanism. The differential reaction of '468-1-1-12' against a number of TYLCD-associated viruses and artificial chimeras between them allowed to identify a region of the virus genome that presumably contains a virus determinant for breaking the resistance to infection observed in '468-1-1-12'.

[Risk of hepatitis B virus transmission from hepatitis B core antibody-positive liver donors]. / Riesgo de transmisión del virus de la hepatitis B de donantes de hígado anti-HBc positivos.

BACKGROUND: To study the hepatitis B virus (HBV) transmission from donors HBsAg-/AntiHBc+ to liver transplant recipients. PATIENTS AND METHOD: We studied retrospectively the HBV serological markers in 43 donors from our center and also the serological condition of the 41 recipients. The HBV serological markers were analyzed by ELISA and HBV DNA was detected by hybridation assays. RESULTS: 13 donors samples showed some HBV serological markers: 6 anti-HBc and anti- HBs (13.9%), 4 anti-HBc (9%) and 3 anti- HBs (6.9%). There were no cases of hepatitis B among liver recipients from donors with negative serological markers. Among the 13 recipients with HBV serological markers, 9 were followed during 39 (SD 17) months. The 5 recipients with no HBV markers, who received an anti- HBc+ with or without anti- HBs (100%) developed hepatitis B. The two liver recipients with anti-HBs solely, did not developed infection (0%). Of the 41 recipients, 15 had some HBV markers before transplant and two of them received an anti-HBc+ and did not develop the infection (0%). CONCLUSIONS: In our study, the prevalence of serological HBV infection in donors and recipients was of 30.2 and 31.7%, respectively. Anti-HBc with or without anti-HBs donors transmitted the HBV infection in all the cases (100%) to the susceptible recipients. The presence of anti-HBs in recipients protected these against the infection. Only the anti-HBs positive donors did not trasmit the HBV infection.

[Hepatitis C virus infection in patients treated with hemodialysis]. / Infección por el virus de la hepatitis C en enfermos tratados con hemodiálisis.

The prevalence of hepatitis C infection was evaluated (Ortho HCV Antibody ELISA Test) in 64 patients with chronic renal failure treated in a single hemodialysis unit. None of these patients was a carrier of hepatitis B virus nor of antibodies against human immunodeficiency virus. Antibodies against hepatitis C virus were detected in 11 patients (17%). The prevalence was higher in the 13 previously diagnosed of non A, non B hepatitis (77%) than in the 51 without previous hepatitis (2%) (p less than 0.001). A relationship between the infection rate and the number of previous blood transfusions was also observed: 5% in the patients without previous transfusions, 13% in the 30 patients who had received between 1 and 10 blood units and 40% in the 15 who had received more than 10 blood units (p less than 0.05). These data suggest that the hepatitis C virus may be responsible for most episodes previously diagnosed as non A, non B hepatitis, and that blood transfusions are the major risk factor.

[Virus and demyelination: why suspect that a virus may be involved in the aetiology of multiple sclerosis?]. / Virus y desmielinización: por qué sospechar la implicacion de virus en la etiología de la esclerosis múltiple?

INTRODUCTION: Epidemiological data indicate that environmental factors, possibly infections, are associated with the development of multiple sclerosis. Different viruses are known to produce demyelination in natural and experimental animal infections. In humans some virus cause acute or chronic diseases that course with central nervous system demyelination. A series of virus have been claimed to be etiological agents of multiple sclerosis, although a causal role for any of them has so far been demonstrated. METHOD: The mechanisms of viral demyelination are diverse,ranging from direct destruction of infected oligodendrocytes to triggering autoimmune responses without virus multiplication in target cells. The potential indirect mechanisms of viral demyelination and the heterogeneous histopathology shown in multiple sclerosis patients, suggesting an heterogeneus etiology, might explain why not a single virus has been as yet identified as the cause of this disease. CONCLUSIONS: Viral infections that cause demyelination in animals and humans are briefly reviewed, focusing on the potential myelin destruction mechanisms and obstacles to the identifying viruses that might cause multiple sclerosis.

Shock cardiogénico por panhipopituitarismo / Cardiogenic shock due to panhypopituitarism

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Measles virus from a long-term persistently infected human T lymphoblastoid cell line, in contrast to the cytocidal parental virus, establishes an immediate persistence in the original cell line.

To investigate the mechanisms of measles virus (MV) establishment and maintenance of persistence in lymphoid cells, we have established a long-term persistent infection with MV, Edmonston strain, in the human T lymphoblastoid cell line MOLT4, which has been in continuous culture for over 8 years. In this culture, designated MOMP1, more than 98% of cells display viral antigens. The MOMP1 culture is immune to superinfection with MV and is not cured by anti-MV antibodies. No evidence of defective interfering particles was obtained. The persistently infected culture releases an infectious virus showing a miniplaque and thermoresistant modified phenotype that, unlike the parental virus Edmonston strain which produces a lytic infection with extensive cell fusion, establishes an immediate persistence in MOLT4 cells with neither significant loss of cell viability nor cell fusion. This suggests that the modification in the virus suffices to maintain the state of persistence without requiring a coevolution of the host cell during the infection, as has been reported in other persistent virus infections.

Measles virus gene expression in lytic and persistent infections of a human lymphoblastoid cell line.

MOMP1 is a measles virus (MV) long-term steady-state persistently infected culture of the human T lymphoblastoid cell line MOLT4. The analysis of MV gene expression revealed that in MOMP1 cells, the major MV proteins, haemagglutinin (H), phosphoprotein (P), nucleoprotein, fusion (F) and matrix (M), are present and the fusion precursor (F0) is cleaved into F2 and F1 peptides. H and F2 proteins are glycosylated in both lytic and persistent MOLT4 infections. All major proteins are underexpressed in the persistently infected cultures in comparison to the lytically infected cells. However a relatively greater reduction was observed for H, M and P proteins. Pulse-chase labelling experiments indicated that this underexpression of H, M and P proteins was not due to selective degradation of these proteins in the persistent infection (p.i.). The relative amounts of the major monocistronic and dicistronic mRNAs for MV proteins, with the exception of P mRNA, was not altered in the p.i. with respect to lytically infected MOLT4 cells, suggesting that the defective expression of H and M proteins was not due to a restriction in the transcription of their mRNAs. In contrast, the mRNA for P protein, the most abundant MV mRNA in these lytically infected T lymphoid cells, is markedly underexpressed in the homologous p.i. Thus the underexpression of P protein in p.i. could be due to a decreased availability of P mRNA. This unbalanced underexpression of MV proteins may impair the cell fusion and c.p.e. of MV and facilitate viral persistence in human lymphoid cells.

Binding of puromycin to E. coli ribosomes. Effects of puromycin analogues and peptide bond formation inhibitors.

(3)H-puromycin binds to bacterial ribosomes, in the presence of ethanol, under the experimental conditions of the fragment reaction assay. The binding is feeble, takes place at 0°C, is partially inhibited by chloramphenicol and lincomycin and totally by sparsomycin. (3)H-puromycin binding is hardly affected by the 3' aminonucleoside of puromycin, is well inhibited by the L-Phenylalanine and L-Leucine analogues of puromycin and totally blocked by L-Phenylalanyl-adenosine.

Kinetic studies of peptide bond formation. Effect of chloramphenicol.

There might be an undetermined order in the interaction of the substrates with the ribosomes in the reaction of CACCA-Leu-Ac with puromycin to form Ac-Leu-puromycin and CACCA ('fragment reaction'). Km 0°=6×10(-4) M for the puromycin · ribosome interaction. Chloramphenicol totally blocks the 'fragment reaction' as a consequence of a single interaction with the ribosome of Kd 0°=2.2×10(-6) M. The inhibition by chloramphenicol of the 'fragment reaction' is mixed competitive for puromycin.

Structural difference between the 5' termini of viral and cellular mRNA in poliovirus-infected cells: possible basis for the inhibition of host protein synthesis.

Host protein synthesis in poliovirus-infected HeLa cells is interrupted, but the host mRNA appears to remain completely intact and unmodified. The average size and poly (A) content of host mRNA was previously known to be unchanged (Koschel, 1974; Leibowitz and Penman, 1971), and this was confirmed. In addition, the 5' terminal methylated "cap" structures remained intact, and no further base modifications at the level of 1 base in 1,000 could be detected. Poliovirus RNA from viruses was previously shown not to have "caps" (Wimmer, 1972), and in this work poliovirus RNA from polyribosomes was found to have pUp at its 5' end. Since, initiation of protein synthesis is probably the basis for the inhibition of cellular protein synthesis in infected cells, the difference in the 5' ends of the host cell and viral RNA could be the basis of selective translation of viral RNA during infection.

5' termini of poliovirus RNA: difference between virion and nonencapsidated 35S RNA.

Poliovirus cytoplasmic, nonencapsidated 35S RNA yields approximately one pUp per molecule upon T2 RNase digestion, indicating that this RNA has the same 5' end as the polyribosome-associated viral RNA fraction. Double-stranded, replicative form RNA after the same treatment yielded approximately four pNp structures per molecule, 65% of which was pUp. In contrast, the 35S RNA from mature virions contained no detectable pNp, indicating that the 5' end of the virion RNA is different from that of the nonencapsidated RNA. None of the above molecules contained pppNp, ppNp, or GpppNp structures present in host mRNA. The virion RNA molecules, as we have shown previously for thenonencapsidated 35S viral RNA (Fernandez-Muñoz and Darnell, 1976), is not labeled with [methyl-3H]methionine.

Intracellular forms of simian virus 40 nucleoprotein complexes. I. Methods of isolation and characterization in CV-1 cells.

A new method was developed for isolation of intracellular forms of simian virus 40 (SV40) nucleoprotein complexes from SV40-infected CV-1 cells late in the infectious cycle. In contrast to the Triton extraction method, which yields only a 60-70S complex, this new procedure yielded three forms of SV40 nucleoprotein complexes: complex I, complex II, and the nature virion (V). The three nucleoprotein complexes differed in physical as well as biochemical properties. Complex I, which is only a small portion of the total SV42 nucleoprotein complexes late during infection, was active in synthesizing both SV40-specific DNA and RNA. Pulse-labeling experiments suggest the following metabolic pathway: I leads to II leads to V. Conversion of complex I to II occurred shortly after the completion of SV40 DNA replication and resulted in the inactivation of the biosynthetic activities of I.

5' Caps in hnRNA: absence of m32,2,7G and size distribution of capped molecules.

In HeLa cells the "small nuclear" RNA has a cap II 5' structure (8)-- m32,2,7G(5') pppXmpYmp-- where X and Y are 2'0 methylated adenosine and uridine. In contrast hnRNA contains only cap I structures were the 2'0 methylated residue may be any base as was earlier reported for cytoplasmic mRNA (8,9,11). With a clear distinction between the source of these two caps an analysis of the size distribution of capped hnRNA could be performed which revealed over 65% of the capped hnRNA molecules were larger than cytoplasmic mRNA.