Showing papers on "Influenza A virus published in 1980"
TL;DR: A longitudinal survey of viruses in feral ducks from 1976 to 1978 in the Vermillion area of Alberta, Canada, has shown that influenza A viruses and paramyxoviruses are present year after year in these apparently healthy ducks.
Abstract: A longitudinal survey of viruses in feral ducks from 1976 to 1978 in the Vermillion area of Alberta, Canada, has shown that influenza A viruses and paramyxoviruses are present year after year in th...
327 citations
TL;DR: Using immunofluorescent staining, it is demonstrated that the target cells of the duck virus in ducks were the simple columnar epithelial cells which form crypts in the large intestines, especially in the colon.
Abstract: Influenza viruses A/duck/Hokkaido/5/77 (Hav7N2), A/budgerigar/Hokkaido/1/77 (Hav4Nav1), A/Kumamoto/22/76 (H3N2), A/Aichi/2/68 (H3N2), and A/New Jersey/8/76 (Hsw1N1) were experimentally inoculated into Pekin ducks. Of these, the influenza viruses of duck and budgerigar origin replicated in the intestinal tract of the ducks. The infected ducks shed the virus in the feces to high titers, but did not show clinical signs of disease and scarcely produced detectable serum antibodies. Using immunofluorescent staining, we demonstrated that the target cells of the duck virus in ducks were the simple columnar epithelial cells which form crypts in the large intestines, especially in the colon. After primary infection, the birds resisted reinfection with the duck virus at least for 28 days, but from 46 days onward they were susceptible to reinfection. These infections were quickly restricted by a brisk secondary immune response, reflected in the rapid appearance of high titers of antibody after reinoculation. In contrat to the avian influenza viruses, the remaining three influenza viruses of human origin did not replicate in the intestinal tract but did cause a serum antibody response.
300 citations
TL;DR: A DNA copy of the gene coding for the influenza A/Aichi/2/68 haemagglutinin protein was cloned in the plasmid pBR322 and the complete nucleotide sequence determined and documents further at the molecular level the two independent modes of antigenic variation of the virus—drift and shift.
Abstract: A DNA copy of the gene coding for the influenza A/Aichi/2/68 haemagglutinin protein was cloned in the plasmid pBR322 and the complete nucleotide sequence determined. Comparison of this primary structure and the deduced amino acid sequence with the haemagglutinin gene and protein of strains belonging to the same (H3) subtype and to different subtypes, of both human (H2) and avian (Hav1) origin, documents further at the molecular level the two independent modes of antigenic variation of the virus--drift and shift.
232 citations
TL;DR: Findings of influenza vaccination in reducing pneumonia and influenza hospitalizations and deaths among elderly members of a prepaid health plan are consistent with those reported in vaccinated young persons, and hence it appears they may be broadly generalized.
Abstract: Effectiveness of influenza vaccination in reducing pneumonia and influenza hospitalizations and deaths among elderly members of a prepaid health plan was analyzed retrospectively. Two epidemics caused by the H3N2 subtype of type A influenza were studied. Vaccine derived from the H2N2 subtype of influenza A virus failed to protect against the Hong Kong (H3N2) virus during the 1968-1969 epidemic. Vaccine derived from the A/Hong Kong/68 (H3N2) virus yielded an estimated 72% (31% to 100%) reduction in hospitalization and 87% (52% to 100%) reduction in mortality during the 1972-1973 epidemic caused by A/England/72 (H3N2). These findings are consistent with those reported in vaccinated young persons, and hence it appears they may be broadly generalized.
229 citations
TL;DR: Because passively transferred maternal antibody to influenza virus may prevent symptomatic infection in young infants, vaccination of pregnant women could be beneficial.
Abstract: Transplacentally acquired antibody to influenza A virus was measured by a microneutralization test and a radioimmunoprecipitation assay in cord blood obtained from infants at a large urban county hospital in 1975-1978. Random samples tested before epidemic periods were a measure of susceptibility of the population. Twenty-six infants from whom cord sera were available had culture-documented infections with influenza A/Victoria (H3N2) virus when younger than four months. The direct correlation between age at the time of infection and level of antibody measured in cord serum (P less than 0.002) suggested a protective effect of transplacentally acquired antibody. None of fourteen acute-phase serum specimens obtained early in the course of culture-positive infections of young infants had detectable antibody to influenza A viral hemagglutinin by the sensitive radioimmunoprecipitation test. Because passively transferred maternal antibody to influenza virus may prevent symptomatic infection in young infants, vaccination of pregnant women could be beneficial.
223 citations
TL;DR: A strategy has been developed for sequencing the single-stranded RNA genes of influenza virus and the nucleotide sequence of segment 7 was completed and provides the primary structure of the matrix protein.
Abstract: A strategy has been developed for sequencing the single-stranded RNA genes of influenza virus. Restriction fragments derived from double-stranded cDNA copies of total influenza RNA were cloned into the bacteriophage M13mp2 and sequenced by the dideoxy technique. Sequences were extended and overlapped by using the virion RNA as template and priming with small restriction fragments. In the course of this strategy, the nucleotide sequence of segment 7 (1027 nucleotides) was completed and provides the primary structure of the matrix protein (27, 861 daltons). In addition, there is a second long reading frame which partly overlaps the reading frame of the matrix protein.
213 citations
TL;DR: If cytotoxic T cells play a role in the protection of humans from influenza, live attenuated vaccines should be considered instead of the currently recommended inactivated virus or subunit vaccines.
Abstract: Subunit and intact influenza A virus vaccines have been compared with infectious virus in a mouse model for their ability to induce memory for cross-reactive cytotoxic T cell responses and to protect mice from challenge with different subtypes of influenza A virus. There is an overall correlation between secondary cytotoxic T cell responses and cross-protection. The most long-lasting and successful cross-protection was observed after intranasal infection with influenza virus A/X31 (H3N2) that replicates efficiently in mice and induces high levels of memory for cross-reactive cytotoxic T cell responses. Short-lasting cross-protection and low levels of T cell-mediated cytotoxicity were associated with infection by A/USSR (H 1N1) virus, that replicates to lower titers in mice, or after multiple injections of inactivated whole virus vaccine. No cross-protection to challenge with heterologous influenza virus was detectable after 1-2 injections of HANA influenza subunit vaccine which failed to prime hosts for cytotoxic T cell responses. These findings may have important implications for vaccination strategy. If cytotoxic T cells play a role in the protection of humans from influenza, live attenuated vaccines should be considered instead of the currently recommended inactivated virus or subunit vaccines.
180 citations
TL;DR: Otitis media developed in 67% of chinchillas inoculated intranasally with type 7 Streptococcus pneumoniae and influenza A virus and suggests that respiratory viral infection contributes significantly to the pathogenesis of acute otitis media.
Abstract: Otitis media developed in 67% of chinchillas inoculated intranasally with type 7 Streptococcus pneumoniae and influenza A virus. Only 4% of chinchillas inoculated with influenza alone and 21% of chinchillas inoculated with S. pneumoniae alone developed otitis media. Among the chinchillas that developed otitis media after inoculation with both pneumococcus and influenza, 73% of the affected ears contained effusion, and 27% of the affected ears showed tympanic membrane inflammation without middle ear effusion obtained on paracentesis. Although a majority of the ears with effusion yielded S. pneumoniae on culture, one-third of the effusions were sterile for aerobic bacteria. This model resembles conditions accompanying otitis media in humans and suggests that respiratory viral infection contributes significantly to the pathogenesis of acute otitis media.
144 citations
TL;DR: Two influenza strains circulating in close temporal association differed in virulence when observed in carefully monitored susceptible populations.
Abstract: Sequential influenza A/Texas/77 (H3N2) and A/USSR/77 (H1N1) epidemics occurred during the winter of 1977-1978 in two populations under viral surveillance for influenza. In college students who reported to the Vanderbilt student health service, roughly equivalent amounts of typical influenzal disease were documented by virus isolation and total health service visits with both strains. However, considering that the college population was fully susceptible to the first introduction of H1N1 virus in 20 years and partially immune to H3N2 viruses through repeated exposure, A/USSR appeared to be a relatively less pathogenic strain. Stronger proof of this was seen in a closely monitored group of 200 largely seronegative infants and young children less than 4 years of age enrolled in an experimental vaccine clinic. In this young population, A/USSR caused no recognizable illness and A/Texas caused typical febrile respiratory disease. Thus, two influenza strains circulating in close temporal association differed in virulence when observed in carefully monitored susceptible populations.
105 citations
TL;DR: The marked degree of antigenic variation of influenza A viruses cannot be explained by an enhanced capacity to produce mutant virions.
104 citations
TL;DR: Intraperitoneal administration of drug begun 72 h after inoculation in regimens equivalent to aerosol afforded less protection than aerosol treatment, and the combination treatment reflected the loss of ribavirin activity.
Abstract: Ribavirin, amantadine, and the two drugs in combination given in small-particle aerosol were highly effective in the treatment of influenza A infection in mice. Treatment was started 72, 96, and 120 h after inoculation and was given continuously for 4 days. With increasing delay in start of treatment, there was a pronounced reduction in effectiveness of ribavirin but not in that of amantadine. The combination treatment reflected the loss of ribavirin activity. Leukocyte infiltration and virus titers in the lungs were inversely related to the effectiveness of treatment. Influenza B infection treated 72 h after inoculation responded only to ribavirin, as indicated by the criteria described for influenza A. Intraperitoneal administration of drug begun 72 h after inoculation in regimens equivalent to aerosol afforded less protection than aerosol treatment.
TL;DR: The results indicate that antigenic variation in the nucleoproteins of influenza A viruses proceeds independently of changes in the viral surface antigens and suggest that point mutations and genetic reassortment may account for nucleoprotein variability.
Abstract: Monoclonal antibodies were used to study antigenic variation in the nucleoprotein of influenza A viruses. We found that the nucleoprotein molecule of the WSN/33 strain possesses at least five different determinants. Viruses of other influenza A virus subtypes showed antigenic variation in these nucleoprotein determinants, although changes in only one determinant were detected in H0N1 and animal strains. The nucleoprotein of human strains isolated from 1933 through 1979 could be divided into six groups, based on their reactivities with monoclonal antibodies; these groups did not correlate with any particular hemagglutinin or neuraminidase subtype. Our results indicate that antigenic variation in the nucleoproteins of influenza A viruses proceeds independently of changes in the viral surface antigens and suggest that point mutations and genetic reassortment may account for nucleoprotein variability.
TL;DR: The nucleotide sequence of the A/PR/8/34 NS gene was determined and found to be the same length (890 nucleotides) as the NS gene of another human influenza virus A/Udorn/72 and of the avian isolate A/FPV/Rostock/34, and is consistent with the findings that the influenza virus NS gene may code for two overlapping polypeptides.
Abstract: The nucleotide sequence of the NS gene of the human influenza virus A/PR/8/34 was determined and found to be the same length (890 nucleotides) as the NS gene of another human influenza virus A/Udorn/72 and of the avian isolate A/FPV/Rostock/34. Comparison of the sequences of the NS genes of the two human influenza viruses shows an 8.9% difference whereas the NS gene of the avian isolate differs by only 8% from that of the human strain A/PR/8/34. The extensive sequence similarity among these three genes does not support the notion of species specific homology groups among NS genes of avian and human influenza virus strains. The primary sequence of the A/PR/8/34 NS gene is consistent with the findings that the influenza virus NS gene may code for two overlapping polypeptides. In addition, an open reading frame potentially coding for a polypeptide 167 amino acids in length was found in the negative strand RNA of the A/PR/8/34 virus NS gene.
TL;DR: Results indicate that the recombinants derived from both donor viruses were satisfactorily attenuated and were stable genetically after replication in doubly seronegative adults although they induced a lower serum hemagglutination inhibition response than that found previously for H3N2 ts and ca recombinant.
Abstract: Two attenuated influenza A donor viruses, the A/Udorn/72 ts-1A2 and the A/Ann Arbor/6/60 cold-adapted (ca) viruses, are being evaluated for their ability to reproducibly attenuate each new variant of influenza A virus to a specific and desired level by the transfer of one or more attenuating genes. Each of these donor viruses has been able to attenuate influenza A viruses belonging to the H3N2 subtype by the transfer of one or more attenuating genes. To determine whether these two donor viruses could attenuate a wild-type virus that belonged to a different influenza A subtype, ts-1A2 and ca recombinants of a wild-type virus representative of the A/USSR/77 (H1N1) Russian influenza strain were prepared and evaluated in adult doubly seronegative volunteers at several doses. The recombinants derived from both donor viruses were attenuated for the doubly seronegative adults. Less than 5% of infected vaccinees developed a febrile or systemic reaction, whereas five of six recipients of wild-type virus developed such a response. The 50% human infectious dose (HID(50)) for each recombinant was approximately 10(5.0) 50% tissue culture infective doses. The virus shed by the ts-1A2 and ca vaccinees retained the ts or ca phenotype, or both. This occurred despite replication of the recombinant viruses for up to 9 days. No evidence for transmission of the ca or ts-1A2 recombinant virus to controls was observed. A serum hemagglutination inhibition response was detected in less than 50% of the infected vaccinees. However, with the more sensitive enzyme-linked immunosorbent assay, a serological response was detected in 100% of the ca vaccinees given 300 HID(50) and approximately 70% of ca or ts vaccinees who received 10 to 32 HID(50) of virus. These results indicate that the recombinants derived from both donor viruses were satisfactorily attenuated and were stable genetically after replication in doubly seronegative adults although they induced a lower serum hemagglutination inhibition response than that found previously for H3N2 ts and ca recombinants.
TL;DR: Nine strains of A/Hong Kong/68 (H3N2) influenza virus, isolated between 1968 and 1977, were examined for changes in amino acid sequences and at least 18 changes occurred in the soluble tryptic peptides of the large haemagglutinin polypeptide (HA1).
Abstract: Haemagglutinin molecules from nine strains of A/Hong Kong/68 (H3N2) influenza virus, isolated between 1968 and 1977, were examined for changes in amino acid sequences. At least 18 changes, 9 of which were located precisely, occurred in the soluble tryptic peptides of the large haemagglutinin polypeptide (HA1) during this period. These peptides contained 262 residues (82% of HA1). In HA2, only two changes in 129 residues (58% of HA2) were detected. Sequential changes at a particular locus were not found; and as far as we can tell, once an amino acid changed, it did not change again in any subsequent variant examined.
TL;DR: Using the dideoxy-chain termination sequencing method with a restriction fragment derived from this clone, it is determined that the 5' ends of matrix gene mRNAs contain a heterogenous sequence of 9-15 nucleotides.
Abstract: Nucleotide sequence analysis of the terminal virus-coded regions of a clone of the matrix gene of influenza virus indicated that the region corresponding to the 5' end of the mRNA contains an additional 13 non-virus coded nucleotides. Using the dideoxy-chain termination sequencing method with a restriction fragment derived from this clone, we have determined that the 5' ends of matrix gene mRNAs contain a heterogenous sequence of 9-15 nucleotides. In addition, the data indicate that the 3' terminal nucleotide of matrix gene virion RNA is not transcribed into mRNA, transcription of influenza virus-specific sequences commencing with the penultimate nucleotide at the 3' end of viron RNA.
TL;DR: The data show that M protein can influence the activity of influenza A virus virion transcriptase and that the susceptibility of influenza virus to rimantadine may be due to the peculiarities of M protein.
Abstract: The transcriptase activity of influenza A virus ribonucleoproteins was inhibited by 42 to 49% in vitro in the presence of membrane (M) protein. The addition of M protein to the system of ribonucleoprotein preparations isolated from rimantadine-sensitive or rimantadine-resistant influenza virus strains, as well as the addition of M protein isolated from a sensitive strain, in the presence of rimantadine further inhibited the transcriptase activity of such complexes by approximately 40%. In the system containing the same ribonucleoprotein preparations, but with M protein isolated from a rimantadine-resistant influenza virus strain, the transcriptase activity was not sensitive to rimantadine. The data show that M protein can influence the activity of influenza A virus virion transcriptase and that the susceptibility of influenza virus to rimantadine may be due to the peculiarities of M protein.
TL;DR: The results suggest that the antigenic variability of influenza viruses may be a consequence of a general genetic variability which effects many of the viral genes.
TL;DR: In epithelial cells, virus budding occurred nearly exclusively at the apical side of the cell surface, but this polarization of virus maturation was found with both pathogenic and nonpathogenic strains, indicating that it does not account for the differences in virus spread and, thus, in pathogenicity.
Abstract: The spread of infection in the chorioallantoic membrane (CAM) has been analysed with pathogenic and non-pathogenic avian influenza A viruses. After allantoic inoculation of pathogenic strains, high titers of infectious virus were found in the allantoic fluid, and virus growth could be demonstrated by immunohistology and electron microscopy in the allantoic epithelium, the mesenchyma, and in the chorionic epithelium. By the same route of inoculation, non-pathogenic strains yielded also high titers of infectious virus in the allantoic fluid, but virus replication was restricted to the allantoic epithelium and did not occur in the other cell layers. After chorionic inoculation of pathogenic strains, replication occurred in all layers of the CAM, and infectious virus was released into the allantoic fluid. However, when the chorionic epithelium was infected with a non-pathogenic strain, infection did not spread beyond the site of inoculation. These differences in virus spread are based on differential activation of the hemagglutinin by proteolytic cleavage. The hemagglutinin of pathogenic strains is cleaved in cells of each layer, whereas the hemagglutinin of non-pathogenic strains is cleaved only in the allantoic epithelium. In epithelial cells, virus budding occurred nearly exclusively at the apical side of the cell surface, but this polarization of virus maturation was found with both pathogenic and nonpathogenic strains, indicating that it does not account for the differences in virus spread and, thus, in pathogenicity.
TL;DR: Use of selected antisera based on clinical history of the patient reduced the cost of rapid viral diagnosis and direct staining of clinical specimens with the commercially available conjugated offered a rapid means of diagnosing respiratory infections on a routine clinical basis when used in conjunction with isolation in tissue culture systems.
Abstract: Staining of clinical respiratory specimens obtained by nasopharyngeal and throat swabs with direct fluorescein isothiocyanate-conjugated antisera to para-influenza virus types 1, 2, and 3, influenza A virus, respiratory syncytial virus, adenovirus, mumps virus, and measles virus was compared with isolation procedures in routine tissue culture systems Direct staining of clinical specimens with the commercially available conjugated offered a rapid means of diagnosing respiratory infections on a routine clinical basis when used in conjunction with isolation in tissue culture systems Of 292 patients who were culture positive for these viruses, 259 were diagnosed by detection of the viral antigen in clinical specimens by direct immunofluorescence No specimens that subsequently yielded a different respiratory virus by culture were positive by the direct immunofluorescence method Use of selected antisera based on clinical history of the patient reduced the cost of rapid viral diagnosis
TL;DR: The nature of the influenza DI viral RNA produced from a single clonal stock was essentially identical in all three cells types, suggesting that these cells do not exert a great selective pressure in the amplification of specific DI viral RNAs either at early or late passages.
Abstract: WSN (H0N1) influenza virus upon undiluted passages in different species of cells, namely, bovine kidney (MDBK), chicken embryo (CEF), and HeLa cells, produced a varying amount of defective interfering (DI) virus which correlated well with the ability of the species of cell to produce infectious virus. However, the nature of the influenza DI viral RNA produced from a single clonal stock was essentially identical in all three cells types, suggesting that these cells do not exert a great selective pressure in the amplification of specific DI viral RNAs either at early or late passages. DI viruses produced from one subtype (H0N1) could interfere with the replication of infectious viruses belonging to other subtypes (H1N1, H3N2). DI viral RNAs could also replicate with the helper function of other subtype viruses. The persistent infection of MDBK and HeLa cells could be initiated by coinfecting cells with both temperature-sensitive mutants (ts-) and DI influenza viruses. Persistently infected cultures cultures at early passages (up to passage 7) showed a cyclical pattern of cell lysis and virus production (crisis), whereas, at later passages (after passage 20), they produced little or no virus and were resistant to infection by homologous virus but not by heterologous virus. The majority of persistently infected cells, however, contained the complete viral genome since they expressed viral antigens and produced infectious centers. Selection of a slow-growing temperature-sensitive variant rather than the presence of DI virus or interferon appears to be critical in maintaining persistent influenza infection in these cells.
TL;DR: The suppression of DTH to the hemagglutinin appears to be mediated by suppressor T cells which carry Lyt-1 membrane antigen marker, and not by sy serum antibody, and the regulation of the immune response to viral infection is discussed.
Abstract: Mice infected with A/England/939/69 X A/Puerto Rico/8/34 (Rec 31) influenza virus by aerosol develop significantly lower levels of delayed-type hypersensitivity (DTH) to A/Hong Kong/1/68 X A/Puerto Rico/8/34/ (X31) virus compared to uninfected mice. The suppression of DTH to the hemagglutinin appears to be mediated by suppressor T cells which carry Lyt-1 membrane antigen marker, and not by sy serum antibody. The suppressor T cells for DTH induced by Rec 31 virus (H3N1) infection suppress the DTH response to the variants of the H3 subtype of influenza viruses, but have no effect on the DTH responses to A/Puerto Rico/8/34 virus (H0N1), a B influenza virus or the matrix protein of type A influenza virus. Suppressor T cells for DTH appear 2 wk after infection and are detectable in the spleen for at least 40 d thereafter. T-helper cells for antibody response to hemagglutinin are induced concomitantly with the T-suppressor cells for DTH. Possible implications of the present findings on the regulation of the immune response to viral infection are discussed.
TL;DR: Six strains of influenza A virus were purified and their proteins were analyzed in a two-dimensional system combining non-equilibrium pH gradient electrophoresis (NEPHGE) with NaDodSO4-polyacrylamide gel electrophorsis, which facilitated the identification of P polypeptides, especially of P2 and P3 whose separation was difficult in a one- dimensional system.
TL;DR: Ribavirin treatment was associated with significantly fewer fourfold or greater rises in antibody to influenza A viral antigen by the complement-fixation test, while rises in hemagglutination-inhibiting antibody titers occurred with equal frequency in both groups.
Abstract: A double-blind placebo-controlled trial of ribavirin was conducted in 97 young adult males naturally infected with influenza virus similar to A/Brazil/11/78 (H1N1). Ribavirin was given orally at a dose of 1,000 mg/day for five days beginning within 24 or 48 hr after onset of clinical influenza. The clinical signs and symptoms of influenza and quantitative viral shedding were the same in ribavirin- and placebo-treated groups. Ribavirin treatment was associated with significantly fewer fourfold or greater rises in antibody to influenza A viral antigen by the complement-fixation test, while rises in hemagglutination-inhibiting antibody titers occurred with equal frequency in both groups. The ribavirin-treated group experienced significant increases in bilirubin and in reticulocyte counts after onset of therapy.
TL;DR: A comparison of the amino acid sequences predicted from the gene sequences for 29C and fowl plague virus haemagglutinins indicates the extent to which changes can occur in the primary sequence of different regions of the protein, while maintaining essential structure and function.
Abstract: The complete nucleotide sequence has been determined for a cloned double-stranded DNA copy of the haemagglutinin gene from the human influenza strain A/NT/60/68/29C, a laboratory-isolated variant of A/NT/60/68, an early strain of the Hong Kong subtype. The gene is 1765 nucleotides long and contains information sufficient to code for a protein of 566 amino acids, which includes a hydrophobic leader peptide (16 residues), HA1 (328), HA2 (221) and an arginine residue which joins the HA subunits. Comparison of the predicted amino acid sequence for 29C haemagglutinin with protein sequence data available for HA from other influenza strains shows that no potential coding information is lost by processing of the mRNA. A comparison of the amino acid sequences predicted from the gene sequences for 29C and fowl plague virus haemagglutinins, (1) indicates the extent to which changes can occur in the primary sequence of different regions of the protein, while maintaining essential structure and function.
TL;DR: Nasopharyngeal washes from 12 patients experimentally infected with influenza A/ Victoria/3/75 wild-type virus were tested in 2 newly developed enzyme-immunoassay (EIA) systems and EIA detected A/Victoria/ 3/75 haemagglutinin antigen for more days than did culture.
TL;DR: Evidence is presented that the antigencic determinants induced by the viral glycoproteins are recognized, in contrast to previous observations that suggested that the M protein of influenza viruses is recognized by these effector cells.
Abstract: Two populations of cytolytic T lymphocytes (CTL) generated after influenza A virus infection can be distinguished into one with specificity for the sensitizing hemagglutinin type and a second with cross-reactivity for antigens induced by other type-A influenza viruses. The molecules carrying the antigenic determinants recognized by the cross-reactive CTL were studied. In L-929 cells abortively infected with fowl plague virus, matrix (M) protein synthesis is specifically inhibited, whereas the envelope glycoproteins, hemagglutinin and neuraminidase, are synthesized and incorporated into the plasma membrane. These target cells were lysed by cross-reactive CTL. The envelope proteins of type A/Victoria virus were separated from the other virion components and reconstituted into lipid vesicles that lacked M protein that subsequently were used to prepare artificial target cells. Target-cell formation with vesicles was achieved by addition of fusion-active Sendai virus. These artificial target cells were also susceptible to lysis by cross-reactive CTL. In contrast to previous observations that suggested that the M protein of influenza viruses is recognized by these effector cells, we present evidence that the antigencic determinants induced by the viral glycoproteins are recognized.
TL;DR: Effector cells that demonstrate delayed‐type hypersensitivity (DTH) on transfer with antigen to naive mice can be recovered from the lungs of mice inoculated intranasally 6 days earlier with a lethal dose (usually 5 × 104EID50) of influenza A virus.
Abstract: Effector cells that demonstrate delayed-type hypersensitivity (DTH) on transfer with antigen to naive mice can be recovered from the lungs of mice inoculated intranasally 6 days earlier with a lethal dose (usually 5x10(1)EID50) of influenza A virus. The activity recovered was proportional to the dose of virus instilled intranasally and the extent of lung consolidation observed. Active cells could also be recovered from the draining lymph nodes and from the peripheral blood. The effector cells were identified as T lymphocytes of Ly 1 phenotype and required I-region sharing between donor and recipient for activity to be elicited. They were cross-reactive within the A group of influenza viruses. Two experiments are reported in which immune cell preparations that expressed DTH activity but had very little cytotoxic T cell activity were transferred to mice inoculated 1 or 2 days earlier with a lethal dose of virus. The mice were not protected from death, and in both experiments, the recipient mice died more rapidly than the controls. These results contrast with earlier results in which cell preparations with high cytotoxic T-cell activity were shown to protect recipient infected mice from death.
TL;DR: The isolation of avian influenza virus from chickens is reported for the second time in the United States since the fowl plague outbreak in 1929 and mortality was moderate, whereas egg production declined markedly.
Abstract: The isolation of avian influenza virus from chickens is reported for the second time in the United States since the fowl plague outbreak in 1929. The Hav6Nl influenza A virus was identified by virus isolation and/or serological techniques from three flocks of commercial Leghorn hens on a single farm in central Minnesota. A fourth house on the same farm was unaffected. Mortality was moderate, whereas egg production declined markedly.
TL;DR: The complete nucleotide sequence of FPV RNA segment 8 largely determined from the cloned DNA predicts two open protein synthesis reading frames that can be translated into polypeptides of sizes similar to those of NS1 and NS2.
Abstract: The smallest RNA segment of influenza A viruses (vRNA segment 8) has recently been shown to code for two unrelated nonstructural proteins (NS1 and NS2) translated from separate mRNAs. Molecular weight considerations indicated that there might not be enough space on vRNA segment 8 for the two coding regions unless they overlap. We have recently cloned in bacterial plasmids several genes of an avian influenza A virus, fowl plague virus (EPV), and now present the complete nucleotide sequence of FPV RNA segment 8 largely determined from the cloned DNA. The DNA sequence predicts two open protein synthesis reading frames that can be translated into polypeptides of sizes similar to those of NS1 and NS2. The coding regions for these polypeptides overlap by the equivalent of 43-60 amino acids, the exact amount depending on which of several possible methionines initiates the synthesis of NS2.