The Recovery of Mice from Influenza Virus Infection: Adoptive Transfer of Immunity with Immune T Lymphocytes

Transfer of primary or secondary influenza-immune spleen cells to mice infected intranasally with influenza virus resulted in a significant clearance of virus from the lungs and the protection of the recipients from death. The antiviral activity was associated only with intact, viable cells and was not due to carryover of virus. The effector cell population responsible for the antiviral effect was shown to be T cells. Thus, the removal of adherent, phagocytic and Ig+ cells did not affect the antiviral activity, whereas it was destroyed with antitheta serum and complement. Antiviral activity was specific and was best expressed if the virus used to infect the recipients and to generate immune cells was the same strain. Further work will be necessary to define rigorously the role of different viral antigens in cell-mediated immune response to influenza virus infection.     

The Recovery of Mice from Influenza A Virus Infection: Adoptive Transfer of Immunity with Influenza Virus-specific Cytotoxic T Lymphocytes Recognizing a Common Virion Antigen

Mice inoculated intranasally with infectious influenza virus of a given A strain were adoptively transferred 24 h later with preparations of secondary influenza virus-immune T cells generated either in vitro or entirely in vivo. The immune cells were raised during infection with homologous or heterologous A strain influenza viruses or with a type B virus. The greatest antiviral effect, measured by reduction in lung virus level of recipient mice, occurred if homologous viruses were used. Sharing of haemagglutinin specificity was shown to be important, but significant antiviral activity was still expressed if neither haemagglutinin nor neuraminidase antigenic specificities were shared. The antiviral effect was type-specific. Adoptive transfer of type A influenza immune T cells did not express antiviral activity against type B virus, and vice versa. On the basis of earlier work, the effector population in the transferred cells was cytotoxic T cells (Tc). Intranasal reinfection of mice with a heterologous type A virus sharing neither haemagglutinin nor neuraminidase antigenic specificity with the first infecting virus induced enhanced and earlier production of cross-reactive Tc against type A influenza viruses. This was paralleled by significantly lower virus levels in the lungs. The results of this work demonstrate heterotypic cell-mediated immunity in influenza virus infection in mice.     

IgA Deficiency and Influenza Infection

A prospective study of influenza infection was carried out on 90 blood donors deficient for serum IgA as tested with double immunodiffusion. Half of them lacked IgA even by radioimmunoassay (RIA). A correlation existed between serum haemagglutination-inhibiting (HI) antibody and resistance to infection, suggesting that the serum HI antibody was an important determinant of protection. The rate of infection as evidenced by a fourfold or greater rise in HI titre, was about the same in the RIA-negative and RIA-positive donors and only slightly higher than the corresponding rate in pregnant women and in a ship's crew.     

Statistics in Infection and Immunity Revisited

In 2003, a review of the use of statistics in Infection and Immunity (IAI) found that more than half of articles had errors of statistical analysis or reporting of statistical results. This updated review of recent articles identifies and discusses the most common statistical methods reported in IAI and provides examples of both good reporting and common mistakes. Furthermore, it expands on the criteria for statistical analysis and reporting presented in the IAI “Instructions to Authors,” with the goal of helping both readers and authors better understand and apply the criteria.     

Prophylaxis and Treatment of Influenza Virus Infection

Influenza virus infections remain an important cause of morbidity and mortality. Furthermore, a recurrence of pandemic influenza remains a real possibility. There are now effective ways to both prevent and treat influenza. Prevention of infection is most effectively accomplished by vaccination. Vaccination with the inactivated, intramuscular influenza vaccine has been clearly demonstrated to reduce serious morbidity and mortality associated with influenza infection, especially in groups of patients at high risk (e.g. the elderly). However, the inactivated, intramuscular vaccine does not strongly induce cell-mediated or mucosal immune responses, and protection induced by the vaccine is highly strain specific. Live, attenuated influenza vaccines administered intranasally have been studied in clinical trials and shown to elicit stronger mucosal and cell-mediated immune responses. Live, attenuated vaccines appear to be more effective for inducing protective immunity in children or the elderly than inactivated, intramuscular vaccines. Additionally, novel vaccine methodologies employing conserved com-ponents of influenza virus or viral DNA are being developed. Preclinical studies suggest that these approaches may lead to methods of vaccination that could induce immunity against diverse strains or subtypes of influenza. Because of the limitations of vaccination, antiviral therapy continues to play an important role in the control of influenza. Two major classes of antivirais have demonstrated ability to prevent or treat influenza in clinical trials: the adaman-tanes and the neuraminidase inhibitors. The adamantanes (amantadine and rimantadine) have been in use for many years. They inhibit viral uncoating by blocking the proton channel activity of the influenza A viral M2 protein. Limitations of the adamantanes include lack of activity against influenza B, toxicity (especially in the elderly), and the rapid development of resistance. The neuraminidase inhibitors were designed to interfere with the conserved sialic acid binding site of the viral neuraminidase and act against both influenza A and B with a high degree of specificity when administered by the oral (oseltamivir) or inhaled (zanamivir) route. The neuraminidase inhibitors have relatively low toxicity, and viral resistance to these inhibitors appears to be uncommon. Additional novel antivirals that target other phases of the life cycle of influenza are in preclinical development. For example, recombinant collectins inhibit replication of influenza by binding to the viral haemagglutinin as well as altering phagocyte responses to the virus. Recombinant techniques have been used for generation of antiviral proteins (e.g. modified collectins) or oligonucleotides. Greater understanding of the biology of influenza viruses has already resulted in significant advances in the management of this important pathogen. Further advances in vaccination and antiviral therapy of influenza should remain a high priority.     

Effect of Influenza Virus Infection on Phagocytic and Cytopeptic Capacities of Guinea Pig Macrophages

Guinea pigs were exposed to influenza Al virus by aerosol. Peritoneal and alveolar macrophages were harvested three days after virus exposure and allowed to attach overnight to Leighton tubes. These macrophages were then challenged with a suspension of Klebsiella pneumoniae for two hours. The macrophages were washed free of extracellular bacteria and antibiotics were added to prevent extracellular multiplication. Plate counts were made at various time intervals on disrupted macrophages to determine the number of viable intracellular bacteria remaining. Alveolar macrophages that had been exposed to virus in vivo ingested the bacteria at a rate significantly greater (p <.05) than that of non-virus exposed control macrophages. However, virus exposed macrophages exhibited significantly reduced intracellular killing (cytopepsis) (p <.01) as compared to controls. In vitro virus exposed macrophages exhibited no significant difference in the rate of phagocytosis or cytopepsis. The data support the hypothesis that virus infection reduces host resistance to bacterial infection by interfering in vivo with cytopepsis of the ingested bacteria.     

Live Victoria/75-ts-1[E] Influenza A Virus Vaccines in Adult Volunteers: Role of Hemagglutinin Immunity in Protection Against Illness and Infection Caused by Influenza A Virus

To explore the relationship between neuraminidase immunity and the degree of attenuatíon of live influenza A virus vaccines, a comparative evaluation of three Victoria/75-ts-1[E] (Vic/75-ts-1[E]) recombinant viruses in serum hemagglutination-inhibiting-negative (titer, 相似文献   

Simian Model for the Evaluation of Immunity to Influenza

Rhesus monkeys (Macaca mulatta) exposed to small-particle aerosols of the Aichi strain of type A2 influenza virus responded by shedding virus from the nasopharynx for 7 to 9 days and by seroconversion (hemagglutination inhibition) 8 or 9 days after exposure. After rechallenge with the homologous virus, no replication of the organism was observed, and a serological anamnestic reaction occurred. The data indicate that the rhesus monkey is a useful primate model for evaluating induced immunity to influenza virus infection.     

Immunity to Influenza in Ferrets: II. Influence of Adjuvants on Immunization

Immunization of ferrets with a single intramuscular inoculation of killed A2/Hong Kong virus did not induce serum or nasal antibody, and these animals were found to be completely susceptible to subsequent infection with virulent influenza virus A2/Hong Kong/3/68. A similar result was found for ferrets immunized with 2 inoculations of killed virus vaccine given 2 weeks apart. Ferrets immunized with killed A2/Hong Kong virus in conjunction with Bordetella pertussis produced relatively low levels of serum HI antibody to A2/Hong Kong virus; when infected with virulent influenza virus, these ferrets showed a modified reaction, with a less marked febrile reaction than was observed for non-immunized animals.Immunization of ferrets with killed A2/Hong Kong virus in Freund''s complete adjuvant resulted in the production of relatively high levels of serum HI antibody, but no detectable nasal antibody. These animals were shown to be partially immune to subsequent infection with virulent influenza virus. However, although the serum antibody levels of these animals following immunization was comparable to that found following infection with live virus, the degree of immunity to infection with virulent influenza virus was measurably less.     

Immunity to Influenza in Ferrets: I. Response to Live and Killed Virus

Ferrets were found to react with a sharp febrile response to intranasal infection with influenza virus A2/Hong Kong/3/68. Virus was recovered from nasal washings taken 3 days after infection, and virus antibody was found in serum specimens taken 21 days after virus infection. Virus infection produced a pronounced rhinitis; the protein concentration in nasal washings was found to increase three to five-fold with peak levels occurring on day 7, post-infection. Concomitant with the increased protein levels, detectable levels of HI and neutralizing antibody were found in the nasal washings. However, nasal washings taken 13 days or more after influenza virus infection did not contain either increased levels of protein or detectable antibody. These ferrets were immune to re-infection with homologous virus inoculated 5 weeks after primary infection. Thus, ferrets showed no febrile response; virus was not recovered from nasal washings; serum antibody titres did not increase; no increase in protein levels was found in nasal washings; and HI antibody was not found in nasal washings.Using these criteria to assess susceptibility or immunity to influenza virus infection, infection with attenuated influenza virus A2/Hong Kong/1/68 produced immunity to re-infection with virulent virus. Ferrets infected with influenza virus B/England/13/65 or immunized with killed A2/Hong Kong virus did not induce any immunity to infection with influenza virus A2/Hong Kong/3/68.     

SARS-CoV-2 Infection: Host Response,Immunity, and Therapeutic Targets

Inflammation - Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has resulted in a global pandemic with severe socioeconomic...     

Influenza Virus Infection and Risk of Acute Myocardial Infarction

Increasing evidences have shown that pathogens might promote atherosclerosis and trigger acute myocardial infarction (AMI). But the conclusions from various studies on the correlation between previous influenza virus (IV) infection and AMI were inconsistent. We conducted a case-control study to assess the association of previous IV infection and AMI. Questionnaire survey was conducted to collect information about demographic characteristics and heart disease risk factors. Fasting blood sample was obtained to measure IgG antibodies to influenza virus A(IV-A), influenza virus B(IV-B), cytomegalovirus (CMV), herpes simplex virus type-1 (HSV-1) and type-2 (HSV-2), adenovirus (ADV), rubella virus (RV) and Chlamydia pneumoniae (CP) and measure the level of some biochemistry markers. Compared to controls, cases were more likely to have positive IgG antibodies to IV-A and IV-B (IV-A: OR, 3.3; 95%CI, 1.5 to 7.4; IV-B: OR, 17.2; 95%CI, 7.7 to 38.0). After adjustment for potential confounding variables, the risk of AMI was still associated with the presence of IgG antibodies to IV-A (adjusted OR, 7.5; 95%CI, 1.3 to 43.0) and IV-B (adjusted OR, 27.3; 95%CI, 6.6 to 113.8). The study supported the hypothesis that previous IV infection took part in the development of atherosclerosis and trigger the occurrence of AMI.     

Dictyocaulus viviparus : Immunological Studies on • Infection: The Immunity Resulting from Experimental Infection

It has been shown experimentally that infection of calves with D. viviparus confers a high degree of resistance to a subsequent reinfection. This acquired immunity can result from a single infection with a sub-lethal dose of larvae or from a series of repeated doses of small numbers of larvae. Animals immunized by a previous infection exhibit on challenge a rapid antibody response and a striking reduction (in some cases to zero) in the numbers of worms reaching the lungs, and in the numbers of larvae appearing in the faeces.