WOUND-TUMOR VIRUS ANTIGENS IN THE INTERNAL ORGANS OF AN INSECT VECTOR.
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Animals↗
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Results for “Virus Internalization”
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[Demonstration and study of the internal proteins of the influenza B virus using solid-phase radioimmunological analysis].
Internal proteins of influenza B/USSR/14/80 virus retaining their antigenic and immunogenic activities were obtained by electrophoresis in 1% agarose. Antisera to eluted NP and M polypeptides were prepared. Study of influenza B viruses isolated in 1940-1984, performed by solid-phase radioimmunoassay, revealed no differences in the antigenic properties of nucleoprotein and matrix protein, except in the B/Yamagata/73 virus.
Electrophoresis, Agar Gel↗
Segregation of an internal biochemical marker during influenza virus recombination and its possible correlation with biological properties.
The internal matrix proteins of A/Okuda/57, A/Finland/4/74 and A/New Jersey/8/76 viruses and several recombinant strains have been examined by radioiodination of the purified proteins followed by peptide mapping. The method is rapid and requires only small amounts of material. Reproducible differences were detected between the matrix proteins of the above parents and allowed the origin of the matrix proteins of the recombinant viruses to be determined. The use of matrix protein identity as a marker in recombination work and its possible correlation with biological properties of the virus is discussed.
Crosses, Genetic↗
Translation of hepatitis A virus RNA in vitro: aberrant internal initiations influenced by 5' noncoding region.
Hepatitis A virus (HAV) RNAs were translated in vitro in rabbit reticulocyte lysates. The pattern of proteins synthesized from full-length HAV RNA was highly complex, consisting of a continuous spectrum of polypeptides ranging from less than 20,000 to greater than 200,000 Da. The pattern was not significantly altered by varying incubation times, ion, or other reaction parameters, or by the addition of HeLa or BS-C-1 cell extracts to the translation reactions. Plasmids engineered with mutations in the 3C coding region produced transcripts which directed the synthesis of the same overall pattern of polypeptide products as those transcribed from wild-type sequences, suggesting that protein processing by 3C did not generate the complex set of protein products. Translation of RNA containing only the P3 coding region of HAV, directly adjacent to the HAV 5' noncoding region, generated a set of protein products which precisely matched a subset of those synthesized from full-length HAV RNA. The translation products of P3 RNA, full-length RNA, and mutant 3C-containing RNAs were analyzed by immunoprecipitation with antisera specific for 3D, VP1, and 2C sequences; several products were subjected to N-terminal sequence analysis. All together, the results demonstrate that translation of HAV RNA in rabbit reticulocyte lysates initiates predominantly at a large number of internal AUG codons, especially those in the P3 coding region. A minor population of products is initiated from sites in the P1 and P2 regions. The latter proteins undergo some proteolytic processing, at unidentified sites, catalyzed by 3C protein sequences. Replacement of the HAV 5' noncoding region with encephalomyocarditis virus 5' end sequences increased initiation at the correct polyprotein start site and both reduced and altered the products generated by internal initiation.
3C Viral Proteases↗
Influenza A viruses with noncleaved hemagglutinin are not internalized after adsorption. Brief report.
Influenza A viruses with noncleaved hemagglutinin (HA) are not internalized after adsorption, since they can be removed and/or inactivated by washing the infected cells at pH 2.5, in contrast to virus with cleaved HA. If uptake of influenza viruses into endosomes is a presupposition for fusion between viral and cellular membranes, this uptake does not occur with virus possessing noncleaved HA.
Adsorption↗
Highly reproducible transient transfections for the study of hepatitis B virus replication based on an internal GFP reporter system.
High throughput studies of hepatitis B virus (HBV) replication are limited by the absence of convenient and reliable in vitro systems that can be utilised to examine mutations emerging as a consequence of selective pressures such as drug therapy, immune response and genotypic evolution. We have developed an efficient and reproducible method of transfecting a human hepatoma cell line (Huh7) with a replication competent clone of HBV, which utilises an internal reporter of transfection efficiency. Wild type (WT) and a common lamivudine (LMV) resistant mutant virus characterised by a methionine to isoleucine mutation in the highly conserved YMDD motif of the polymerase gene were used to highlight the utility of this in vitro transfection procedure in studying common HBV mutations. The presence of an internal GFP reporter increased the efficiency of generating highly reproducible results and facilitated multiple forms of analysis from a single transfection accurately.
Antiviral Agents↗
Mode of delivery and postpartum morbidity in Latin American and Caribbean countries among women who are infected with human immunodeficiency virus-1: the NICHD International Site Development Initiative (NISDI) Perinatal Study.
OBJECTIVE: The purpose of this study was to test whether cesarean delivery before labor and before ruptured membranes is associated with a higher risk of postpartum morbidity than vaginal delivery among women who are infected with human immunodeficiency virus-1 in Latin America and the Caribbean. STUDY DESIGN: Data from a prospective cohort study (National Institute of Child Health and Human Development International Site Development Initiative Perinatal Study) were analyzed. The study population consisted of women who were followed for > or = 6 to 12 weeks after delivery, who had singleton infants, and with a known mode of delivery. RESULTS: Of 819 enrollees, 697 women met inclusion criteria (299 vaginal deliveries, 260 cesarean deliveries before labor and before ruptured membranes, 138 cesarean deliveries after labor and/or after ruptured membranes); 36 women (5%) had postpartum morbidity (18 major, 18 minor). Mode of delivery was associated with postpartum morbidity (P = .02). Unadjusted odds ratios (95% CIs) for postpartum morbidity according to mode of delivery were cesarean delivery before labor and before ruptured membranes (odds ratio, 1.16 [95% CI, 0.5, 2.7]), cesarean delivery after labor and/or after ruptured membranes (odds ratio, 2.96 [95% CI, 1.3, 6.7]), and vaginal delivery (reference). These results did not differ appreciably with covariate adjustment. CONCLUSION: The rate of postpartum morbidity was low. Mode of delivery was associated with postpartum morbidity, possibly reflecting the larger proportion of minor postpartum morbidity events among those with cesarean delivery after labor and/or after ruptured membranes.
Adult↗
Acutely infected Langerhans cells are more efficient than T cells in disseminating HIV type 1 to activated T cells following a short cell-cell contact.
Most human immunodeficiency virus type 1 (HIV-1) infections involve sexual contact and virus passage across mucosal surfaces. While Langerhans cells (LCs) and dendritic cells (DCs) have been implicated in mucosal infection, their role is undefined. Here we demonstrate that acutely HIV-1-infected LCs and DCs effectively transmit virus to uninfected, activated T cells. Cocultivation of these cells results in massive virus production that requires a short cell-cell contact; as little as 30 min contact time is sufficient for HIV-1-pulsed DCs to infect their target T cells. Furthermore, surface-bound virus inactivation by trypsin does not significantly decrease the efficiency of virus transmission by LC/DCs, suggesting rapid internalization of virus. This effective virus transfer by infected LCs and blood-derived DCs requires prior activation of T cells. Surprisingly, cocultivation of acutely infected T cells with uninfected, activated target T cells results only in low virus production, even with T cell-tropic virus. We conclude that LCs and DCs are not only important targets of HIV-1 infection, but may also play a key role in the early dissemination of virus to T cells they encounter in skin or lymphoid tissue.
Cells, Cultured↗
Temporal gating of nuclear import: How Merkel cell polyomavirus exploits the cell cycle for nuclear entry.
Merkel cell polyomavirus (MCPyV) is a small, DNA tumor virus that is causally linked to an aggressive form of human skin cancer called Merkel cell carcinoma. MCPyV is the only polyomavirus definitively shown to cause cancer in humans, yet little is known about how it establishes infection in target cells. In this study, we report an unconventional mechanism by which MCPyV enters the host cell nucleus, where viral genome replication occurs. We demonstrate that, unlike other known polyomaviruses, MCPyV does not require the nuclear pore complex during entry. Instead, it takes advantage of cell cycle-dependent nuclear envelope breakdown to deliver its genetic material into the nucleus. We further show that the VP1 major capsid protein is sufficient to facilitate this process. Overall, our findings reveal a novel mechanism of polyomavirus nuclear entry and provide insight into the diverse mechanisms that these viruses use to cause infection.
Merkel cell polyomavirus↗
[Taxonomy of viruses, 1975].
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DNA Viruses↗
Regulation of the mouse mammary tumor virus receptor by phosphorylation and internalization in mammary epithelial cells.
The mouse mammary tumor virus enters mammary epithelial cells via a plasma membrane protein that binds to a viral envelope glycoprotein, gp52. In intact cells, this gp52 receptor can be phosphorylated by activators of protein kinase A and protein kinase C (PKC), but this modification does not occur in response to epidermal growth factor, whose receptor is a tyrosine kinase, or to gp52. Phosphorylation of the gp52 receptor rapidly leads to internalization and gradual loss of binding activity. Both the phosphorylation and the internalization induced by PKC are abolished by prior downregulation of this kinase. Although the physiological function of the gp52 receptor is unknown, its binding to gp52 can stimulate several biological activities, including amino acid accumulation. Receptor processing impairs this gp52-induced amino acid uptake, as well as viral infection, by depleting the binding protein at the cell surface. In contrast, PKC augments insulin-induced amino acid transport, and PKC downregulation abolishes the action of insulin, suggesting that insulin and gp52 utilize partially separate pathways leading to amino acid transport. These data further suggest that PKC may be involved in this insulin-stimulated activity.
Aminoisobutyric Acids↗
Evaluation of twenty human adenoviral types and one infectivity-enhanced adenovirus for the therapy of soft tissue sarcoma.
The clinical course of sarcoma warrants the development of new therapeutic options, such as gene therapy. However, the lack of coxsackievirus-adenovirus receptor (CAR) on sarcoma cells limits the efficacy of adenovirus type 5 (Ad5)-based gene therapy. In this study we evaluated 20 different adenoviral types and 1 Ad5 vector with RGD-containing fiber for their internalization efficiency in sarcoma cells. We demonstrated that adenovirus types 35, 3, 7, 11, 9, and 22 and Ad5lucRGD virions (ranked in descending order) have significantly higher internalization efficiency in the tested sarcoma cells when compared with Ad5. On the basis of these results we developed a conditionally replication-competent adenoviral vector, Ad5Delta24.Ki.COX, and compared its oncolytic efficacy with that of Ad5/35Delta24.Ki.COX, an Ad5-based vector with the Ad35 fiber shaft and knob domains. Because both vectors differed only in the fiber, we were able to assess whether the adenoviral type with the most efficient internalization resulted also in enhanced treatment efficacy. We evaluated the antineoplastic activity of the oncolytic adenoviral vectors alone or in combination with the expression of measles virus fusogenic membrane glycoproteins and/or ifosfamide. The findings of our xenograft model were as follows: animals that received Ad5/35-based therapy had significantly smaller tumors than animals treated with the homologous Ad5-based vectors. In addition, we demonstrated that the combination of virotherapy, intratumoral expression of fusogenic membrane glycoproteins, and ifosfamide was clearly superior compared with treatment with individual components alone or as combinations of two components. In conclusion, Ad35-based vectors are promising for the treatment of sarcoma.
Adenoviridae↗
Naturally occurring dicistronic cricket paralysis virus RNA is regulated by two internal ribosome entry sites.
Cricket paralysis virus is a member of a group of insect picorna-like viruses. Cloning and sequencing of the single plus-strand RNA genome revealed the presence of two nonoverlapping open reading frames, ORF1 and ORF2, that encode the nonstructural and structural proteins, respectively. We show that each ORF is preceded by one internal ribosome entry site (IRES). The intergenic IRES is located 6,024 nucleotides from the 5' end of the viral RNA and is more active than the IRES located at the 5' end of the RNA, providing a mechanistic explanation for the increased abundance of structural proteins relative to nonstructural proteins in infected cells. Mutational analysis of this intergenic-region IRES revealed that ORF2 begins with a noncognate CCU triplet. Complementarity of this CCU triplet with sequences in the IRES is important for IRES function, pointing to an involvement of RNA-RNA interactions in translation initiation. Thus, the cricket paralysis virus genome is an example of a naturally occurring, functionally dicistronic eukaryotic mRNA whose translation is controlled by two IRES elements located at the 5' end and in the middle of the mRNA. This finding argues that eukaryotic mRNAs can express multiple proteins not only by polyprotein processing, reinitiation and frameshifting but also by using multiple IRES elements.
Animals↗
Receptors mediating adenovirus attachment and internalization.
Adenovirus infection requires that the virus attach to cells and be internalized. Interaction between the viral fiber protein and specific cell surface receptors, such as the 46-kDa coxsackievirus and adenovirus receptor (CAR), is responsible for attachment; a second interaction between the viral penton base and cell surface integrins facilitates virus internalization. Expression of receptors may determine whether tissues are susceptible to adenovirus infection and adenovirus-mediated gene delivery.
Adenoviridae↗
U.S. Public Health Service (PHS) consultation on international collaborative human immunodeficiency virus (HIV) research.
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Beneficence↗
The low tumorigenic potential of PRCII, among viruses of the Fujinami sarcoma virus subgroup, corresponds to an internal (fps) deletion of the transforming gene.
The avian sarcoma viruses FSV, PRCII, PRCIIp, and PRCIV share a related class of hybrid onc genes (delta gag-fps) defined by a specific nucleotide sequence fps and by delta gag-fps proteins of different sizes. Among these viruses, PRCII appears to have a lower tumorigenic potential than the others. Here we have compared fibroblast-transforming function and onc gene structure of these viruses. The fibroblast transforming ability of PRCII was lower than those of FSV, PRCIIp, and PRCIV. By gel electrophoresis the genomic RNA of PRCII measured 3.5 kb and those of FSV, PRCIIp, and PRCIV 4.5 kb; the delta gag-fps protein of PRCII measured 105 kilodaltons (kd), that of FSV 140 kd, and those of PRCIIp and PRCIV about 150 kd. By fingerprinting viral RNAs hybridized with molecularly cloned viral DNA the delta gag regions of PRCII and PRCIIp were defined to be 1.45 kb and that of FSV to be 1.3 kb. Fingerprint analysis of viral RNA-proto fps DNA hybrids showed the fps regions (approximately 2.8 kb) of FSV and PRCIIp to be isogenic. Compared to FSV and PRCIIp, the fps sequence of PRCII lacked a 1-kb region which maps between 0.3 and 1.3 kb from the 5' end of fps in FSV and PRCIIp. Based on oligonucleotide analysis, the shared fps complements of PRCII and PRCIIp were indistinguishable while that of FSV differed from those of the PRC viruses in scattered point mutations amounting to 1-2% of the RNA. Since all other regions of PRCII are isogenic with those of the highly tumorigenic variants PRCIIp, PRCIV, and FSV, it is concluded that the low fibroblast-transforming and oncogenic potential of PRCII reflects the internal fps deletion. Since the fps deletion reduces but does not eliminate transforming function, we suggest that the complete onc genes of viruses in the FSV subgroup include either several functional, or a regulatory and a functional fibroblast transforming domain. It has been reported that the 3' domains of the onc genes of viruses in the Fujinami subgroup and the onc genes of certain feline sarcoma viruses are distantly related. Since full transforming potential of the avian viruses depends on the 5' fps region not shared with the feline sarcoma viruses, we suggest that despite their structural homology, the avian and feline onc genes must have functionally different domains.
Animals↗
Abortive infection with Sindbis virus of a Chinese hamster ovary cell mutant defective in phosphatidylserine and phosphatidylethanolamine biosynthesis.
The effects of phosphatidylserine starvation on the infection with Sindbis virus (an enveloped RNA virus) have been investigated in a Chinese hamster ovary (CHO) cell mutant (strain PSA-3) which requires exogenously added phosphatidylserine for cell growth because it lacks the ability to synthesize this phospholipid. When PSA-3 cells were grown in the absence of phosphatidylserine, the cellular contents of phosphatidylserine and also phosphatidylethanolamine produced through decarboxylation of phosphatidylserine decreased. Sindbis virus production in the mutant cells decreased immediately upon phosphatidylserine deprivation as did the contents of phosphatidylserine and phosphatidylethanolamine, whereas the cell growth, viability, and syntheses of protein, DNA and RNA remained normal for approx. 40 h phosphatidylserine starvation. Although PSA-3 cells grown without phosphatidylserine for 24 h were able to bind and internalize Sindbis virus almost normally, viral RNA synthesis was greatly reduced in the cells, suggesting that nucleocapsids of internalized Sindbis virus are not normally released into the cytoplasm. Unlike mammalian cell mutants defective in endosomal acidification, PSA-3 cells grown without phosphatidylserine were not resistant to diphtheria toxin. Furthermore, the yield of virions and viral RNA synthesis in PSA-3 cells were not completely restored on brief exposure of the cells to low pH medium following virus adsorption, which is known to induce artificial fusion of the viral envelope with the plasma membrane of normal host cells and then injection of viral nucleocapsids into the cytoplasm. Our data demonstrate the requirement of membrane phospholipids, such as phosphatidylserine and/or phosphatidylethanolamine, in CHO cells for Sindbis virus infection, and we discuss their possible roles.
Animals↗