gsgs
Registered User
55 children followed from birth, 44 other children, 85 adults 1975-1981 ,Houston, only H3N2.
P(1977f | 1976f) = 63% , P(1980f | 1977f and 1976f) >0
P(1980f | 1977f but not before) = "little or no" ~ 1/19
P(1978-81 , H1N1) ~ 1/19
P(1978f | none before) = big, not protected
P(1979f) = smaller,
socioeconomic and other factors influencing intensity of exposure
age at primary infection
varying degrees of antigenic difference between sequential variants of a major subtype
unrecognized immunogenicity or virulence differences between subtypes and variants.
are there seroprevalence tests after the 1957 or 1968 pandemics ?
Did non-vaccinated people who had no infection develope immunity ?
http://www.sma.org.sg/smj/4001/articles/4001e1.html
http://www.pubmedcentral.nih.gov/art...?artid=1129512
http://www.ncbi.nlm.nih.gov/sites/en...indexed=google
From the last article:
Variation in frequency of natural reinfection with influenza A viruses.
Frank AL, Taber LH.
To investigate the frequency of natural reinfection with influenza A viruses, 55 children followed from birth along with the 44 other children and 85 adults in their families were observed for varying periods between 1975 and 1981 in the Houston Family Study. Persons infected in 1976 or early 1977 with influenza A subtype H3N2 experienced a high rate of reinfection during the 1977-78 season (63% in one group of young children) and additional reinfections in 1980-81. Persons in whom H3N2 infection was first observed in 1977-78 had little or no reinfection in 1980-81; one reinfection was observed in 1980-81 among 19 young children at risk. Only one reinfection with influenza A subtype H1N1 was observed following introduction of the virus in early 1978 despite exposure in 1978-80 and a substantial outbreak in 1980-81. Statistically significant protection from reinfection in young children followed from birth was not noted for the 1977-78 H3N2 outbreak but was present in 1979-81 for both H3N2 and H1N1 viruses. Reasons for variations in reinfection suggested by this data include 1) socioeconomic and other factors influencing intensity of exposure, 2) age at primary infection, 3) varying degrees of antigenic difference between sequential variants of a major subtype, and 4) unrecognized immunogenicity or virulence differences between subtypes and variants.
PMID: 6619811 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/e...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Nov.2005
It is generally believed that the production of influenza-specific IgG in response to viral infection is dependent on CD4 T cells. However, we previously observed that CD40-deficient mice generate influenza-specific IgG during a primary infection, suggesting that influenza infection may elicit IgG responses independently
of CD4 T cell help. In the present study, we tested this hypothesis and show that mice
lacking CD40 or CD4 T cells produce detectable titers of influenza-specific IgG and recover
from influenza infection in a manner similar to that of normal mice.
In contrast, mice completely lacking B cells succumb to influenza infection,
despite the presence of large numbers of functional influenza-specific CD8 effector cells
in the lungs. Consistent with the characteristics of a T-independent Ab response,
long-lived influenza-specific plasma cells are not found in the bone marrow of CD40-/- and
class II-/- mice, and influenza-specific IgG titers wane within 60 days postinfection.
However, despite the short-lived IgG response, CD40-/- and class II-/- mice are
completely protected from challenge infection with the same virus administered
within 30 days. This protection is mediated primarily by B cells and Ab,
as influenza-immune CD40-/- and class II-/- mice were still resistant to challenge infection when T cells were depleted. These data demonstrate that T cell-independent influenza-specific Ab promotes the resolution of primary influenza infection and helps to prevent reinfection.
http://www.ncbi.nlm.nih.gov/sites/e...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
1: Am J Epidemiol. 1982 Aug;116(2):212-27. Links
Influenzavirus infections in Seattle families, 1975-1979. I. Study design, methods and the occurrence of infections by time and age.Fox JP, Hall CE, Cooney MK, Foy HM.
Intensive surveillance of Seattle, Washington, families with school-age children for influenzavirus infections during 1975-1979 encompassed 639 family- and 2732 person-seasons of observation, covering four influenzavirus epidemic seasons: type B (1975-1979), type A/H3N2 (1975-1976 and 1977-1978) and type A/H1N1 (1978-1979). Late spring "herald" waves of infection occurred in 1977 (A/H3N2), 1978 (A/H1N1) and 1979 (type B), the latter presaging an epidemic in 1979-1980. Out-of-season infections, recognized by serology only, included type B and A/H3N2 viruses in each summer and A/H1N1 virus in 1978. In epidemic seasons, infection rates were highest in children aged 5-9 years (A/H3N2) or in teenagers (A/H1N1 and type B). A/H1N1 virus caused the sharpest epidemic, with 31% of the population (but only 2% of adults) infected and 72% of households invaded in 1978-1979. These compare with infection rates of 17-24% overall and 6-13% of adults and the invasion of 38-53% of households observed in the type B and two A/H3N2 epidemics. Extended observation (largely serologic) of a cohort of 1965-1969 Virus Watch families for up to 14 years (including one three-year gap) indicated overall infection rates of 13.7 and 16.4 per 100 person-years with types B and A/H3N2 viruses, respectively, and rates of first and second reinfections of about 3 and 1 per 100 person-years, respectively, with each virus. Close surveillance in 1975-1979 revealed second family episodes of infection with each prevalent virus, 37 with A/H3N2, 15 with type B and 13 with A/H1N1 virus. Risk of infection in these episodes was related more to current hemagglutination-inhibiting titers than to experience (infected or not) in the initial episodes, with 67-100% reinfection when titers were low. Among younger (less than 20 years old) members, related illness was as frequent with reinfection as with initial infection.
PMID: 7114033 [PubMed - indexed for MEDLINE]
1: Infect Immun. 1976 Feb;13(2):417-24. Links
Influenza infection in ferrets: role of serum antibody in protection and recovery.Small PA, Waldman RH, Bruno JC, Gifford GE.
The passive administration of ferret antiserum to Ao (H0N1) influenza virus failed to protect the recipient ferrets from subsequent infection with homologous virus. This susceptibility to infection was observed even when the passively acquired serum hemagglutination inhibition (HI) titer was similar to peak convalescent titers. It is therefore concluded that serum antibody alone is probably not a major factor in the prevention of influenza infection. This does not rule out a possible role for serum antibody in prevention of illness. Subsequent to infection, ferrets that had received passive antisera failed to develop high levels of serum HI antibody. In fact, many had no detectable serum antibody (less than 1:8). These animals shed virus for periods of time quite similar to those of infected control animals, which did develope serum antibody. From these data it was concluded that detectable serum HI antibody does not play a significant role in the recovery of ferrets from influenza infection. Interferon was present in high concentrations in the secretions a few days prior to cessation of virus shedding, but it is not clear whether this was the cause of the recovery or merely a concomitant event. Twenty-one days after initial infection two-thirds of the ferrets that had received passive antibody and all control animals were immune to reinfection with the homologous influenza virus. Since the former group had little or no detectable serum HI antibody but most members were immune, there must be some other host mechanism to account for the immunity.
PMID: 1262059 [PubMed - indexed for MEDLINE]
------------------------------------------
Antibody responses persisting at least 7 mo following immunization were demonstrated in 70% of 428 vaccinated young adults for A2 antigen and 20% for influenza B antigen.
P(1977f | 1976f) = 63% , P(1980f | 1977f and 1976f) >0
P(1980f | 1977f but not before) = "little or no" ~ 1/19
P(1978-81 , H1N1) ~ 1/19
P(1978f | none before) = big, not protected
P(1979f) = smaller,
socioeconomic and other factors influencing intensity of exposure
age at primary infection
varying degrees of antigenic difference between sequential variants of a major subtype
unrecognized immunogenicity or virulence differences between subtypes and variants.
are there seroprevalence tests after the 1957 or 1968 pandemics ?
Did non-vaccinated people who had no infection develope immunity ?
http://www.sma.org.sg/smj/4001/articles/4001e1.html
http://www.pubmedcentral.nih.gov/art...?artid=1129512
http://www.ncbi.nlm.nih.gov/sites/en...indexed=google
From the last article:
Variation in frequency of natural reinfection with influenza A viruses.
Frank AL, Taber LH.
To investigate the frequency of natural reinfection with influenza A viruses, 55 children followed from birth along with the 44 other children and 85 adults in their families were observed for varying periods between 1975 and 1981 in the Houston Family Study. Persons infected in 1976 or early 1977 with influenza A subtype H3N2 experienced a high rate of reinfection during the 1977-78 season (63% in one group of young children) and additional reinfections in 1980-81. Persons in whom H3N2 infection was first observed in 1977-78 had little or no reinfection in 1980-81; one reinfection was observed in 1980-81 among 19 young children at risk. Only one reinfection with influenza A subtype H1N1 was observed following introduction of the virus in early 1978 despite exposure in 1978-80 and a substantial outbreak in 1980-81. Statistically significant protection from reinfection in young children followed from birth was not noted for the 1977-78 H3N2 outbreak but was present in 1979-81 for both H3N2 and H1N1 viruses. Reasons for variations in reinfection suggested by this data include 1) socioeconomic and other factors influencing intensity of exposure, 2) age at primary infection, 3) varying degrees of antigenic difference between sequential variants of a major subtype, and 4) unrecognized immunogenicity or virulence differences between subtypes and variants.
PMID: 6619811 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/e...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Nov.2005
It is generally believed that the production of influenza-specific IgG in response to viral infection is dependent on CD4 T cells. However, we previously observed that CD40-deficient mice generate influenza-specific IgG during a primary infection, suggesting that influenza infection may elicit IgG responses independently
of CD4 T cell help. In the present study, we tested this hypothesis and show that mice
lacking CD40 or CD4 T cells produce detectable titers of influenza-specific IgG and recover
from influenza infection in a manner similar to that of normal mice.
In contrast, mice completely lacking B cells succumb to influenza infection,
despite the presence of large numbers of functional influenza-specific CD8 effector cells
in the lungs. Consistent with the characteristics of a T-independent Ab response,
long-lived influenza-specific plasma cells are not found in the bone marrow of CD40-/- and
class II-/- mice, and influenza-specific IgG titers wane within 60 days postinfection.
However, despite the short-lived IgG response, CD40-/- and class II-/- mice are
completely protected from challenge infection with the same virus administered
within 30 days. This protection is mediated primarily by B cells and Ab,
as influenza-immune CD40-/- and class II-/- mice were still resistant to challenge infection when T cells were depleted. These data demonstrate that T cell-independent influenza-specific Ab promotes the resolution of primary influenza infection and helps to prevent reinfection.
http://www.ncbi.nlm.nih.gov/sites/e...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
1: Am J Epidemiol. 1982 Aug;116(2):212-27. Links
Influenzavirus infections in Seattle families, 1975-1979. I. Study design, methods and the occurrence of infections by time and age.Fox JP, Hall CE, Cooney MK, Foy HM.
Intensive surveillance of Seattle, Washington, families with school-age children for influenzavirus infections during 1975-1979 encompassed 639 family- and 2732 person-seasons of observation, covering four influenzavirus epidemic seasons: type B (1975-1979), type A/H3N2 (1975-1976 and 1977-1978) and type A/H1N1 (1978-1979). Late spring "herald" waves of infection occurred in 1977 (A/H3N2), 1978 (A/H1N1) and 1979 (type B), the latter presaging an epidemic in 1979-1980. Out-of-season infections, recognized by serology only, included type B and A/H3N2 viruses in each summer and A/H1N1 virus in 1978. In epidemic seasons, infection rates were highest in children aged 5-9 years (A/H3N2) or in teenagers (A/H1N1 and type B). A/H1N1 virus caused the sharpest epidemic, with 31% of the population (but only 2% of adults) infected and 72% of households invaded in 1978-1979. These compare with infection rates of 17-24% overall and 6-13% of adults and the invasion of 38-53% of households observed in the type B and two A/H3N2 epidemics. Extended observation (largely serologic) of a cohort of 1965-1969 Virus Watch families for up to 14 years (including one three-year gap) indicated overall infection rates of 13.7 and 16.4 per 100 person-years with types B and A/H3N2 viruses, respectively, and rates of first and second reinfections of about 3 and 1 per 100 person-years, respectively, with each virus. Close surveillance in 1975-1979 revealed second family episodes of infection with each prevalent virus, 37 with A/H3N2, 15 with type B and 13 with A/H1N1 virus. Risk of infection in these episodes was related more to current hemagglutination-inhibiting titers than to experience (infected or not) in the initial episodes, with 67-100% reinfection when titers were low. Among younger (less than 20 years old) members, related illness was as frequent with reinfection as with initial infection.
PMID: 7114033 [PubMed - indexed for MEDLINE]
1: Infect Immun. 1976 Feb;13(2):417-24. Links
Influenza infection in ferrets: role of serum antibody in protection and recovery.Small PA, Waldman RH, Bruno JC, Gifford GE.
The passive administration of ferret antiserum to Ao (H0N1) influenza virus failed to protect the recipient ferrets from subsequent infection with homologous virus. This susceptibility to infection was observed even when the passively acquired serum hemagglutination inhibition (HI) titer was similar to peak convalescent titers. It is therefore concluded that serum antibody alone is probably not a major factor in the prevention of influenza infection. This does not rule out a possible role for serum antibody in prevention of illness. Subsequent to infection, ferrets that had received passive antisera failed to develop high levels of serum HI antibody. In fact, many had no detectable serum antibody (less than 1:8). These animals shed virus for periods of time quite similar to those of infected control animals, which did develope serum antibody. From these data it was concluded that detectable serum HI antibody does not play a significant role in the recovery of ferrets from influenza infection. Interferon was present in high concentrations in the secretions a few days prior to cessation of virus shedding, but it is not clear whether this was the cause of the recovery or merely a concomitant event. Twenty-one days after initial infection two-thirds of the ferrets that had received passive antibody and all control animals were immune to reinfection with the homologous influenza virus. Since the former group had little or no detectable serum HI antibody but most members were immune, there must be some other host mechanism to account for the immunity.
PMID: 1262059 [PubMed - indexed for MEDLINE]
------------------------------------------
Antibody responses persisting at least 7 mo following immunization were demonstrated in 70% of 428 vaccinated young adults for A2 antigen and 20% for influenza B antigen.