Pathology

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The influenza virus may be the most dangerous virus in the world. Several times in past history, this virus has been responsible for killing huge numbers of people within a 1 to 2 year period. As an example, the "Spanish Flu" /type A(H1N1) of 1918-19 killed about 500,000 people in the United States and at least 20 million people worldwide. In 1957-58, the "Asian Flu" /type A(H2N2) resulted in 70,000 deaths in the United States and in 1968-69, the "Hong-Kong Flu" /type (A(H3N2) killed 34,000 in the United States.

Epidemic influenza is divided into type A and type B. The most common presentation of influenza includes a fever (usually 100-103 degrees F in adults), respiratory symptoms (such as cough, sore throat, runny or stuffy nose), headache, muscle aches, and often extreme fatigue.

In an average year, influenza is associated with about 20,000 deaths, especially for the elderly, immuno-compromised, or those who have an existing condition, such as asthma, diabetes or heart disease.

Currently there are three main variants circulating, two type "A" and one type "B". The type A variants are the "Hong Kong" /type A(H3N2) virus and its relatives, responsible for about 400,000 deaths in the United States since 1968 and distant relatives of the "Spanish Flu", type A(H1N1). There is considerable concern that the Avian Flu (H5N1) could cross species and cause a worlwdie pandemic.

The "H" and "N" refer to viral proteins called haemagglutinin and the neuraminidase.

The influenza viruses are able to mutate or change over time, allowing them to reinfect year after year. Usually this is a slow and very gradual process; both type A and B influenza virus can change in this manner. However, every once in a while, the type A strains will have a dramatic and abrupt change to either its haemagglutinin and/or neuraminidase proteins. This results in a new strain of the virus.

Blood groups and influenza

Quite a few different researchers have investigated blood group and influenza.

After exposure to the influenza virus, an immune process termed "seroconversion" takes place in which the immune system attempts to produce antibodies to the virus.. Researchers have found that after circulation of influenza A (type (H1N1) and (H3N2))(1) and influenza B viruses, the immune response (as measured in a rise in antihaemagglutinin antibodies against the virus) differ between the blood groups.(2)

Blood group characteristics to seroconversion

  • Blood group A in general has a greater ability to generate a quick and substantial antibody response against influenza type A(H1N1) and especially A(H3N2).(3) Their antibody response against influenza B is not quite as dramatic.(4)
  • Blood group AB has a relatively poor ability to generate high antibody levels against any of the influenza viruses.
  • Blood group B: Reasonable ability to generate an antibody response against influenza A(H1N1). Slowest (3-5 months) and weakest ability to generate antibodies against influenza A(H3N2)(5) of any blood group. Against influenza B virus, blood group B has a significant advantage and responds differently from either blood group A or O. The blood group B immune response happens much earlier and persists longer.(6)
  • Blood group O: Modest ability to generate antibody response against influenza A(H1N1) and A(H3N2) viruses. Antibody response against influenza B is not as dramatic as blood group B.

Some researchers have hypothesized that one explanation for the typical emergence of the new epidemic strains of influenza in Asia is connected to blood group and the relatively high proportion of group blood found in Asia. It would appear that blood group B has a genetic predisposition to latent (chronic) persistence of influenza A virus (especially A(H3N2) "Hong Kong" variants). Often, the influenza virus antigen can still be found in healthy group B individuals as long as 5 months after infection.(7)

People with blood group B (and AB) can expect to be much more susceptible to infection during times when new antigenic variants and serotypes of influenza virus appear. This is actually particularly bad news since this is the type of influenza A virus change that results in widespread flu pandemics. Blood group O individuals tend to be susceptible to influenza infection at the period of the circulation of virulent strains (so in years when the flu is making people feel really sick, type O will be hit the hardest). Blood group A has a generalized susceptibility to the less virulent strains of influenza A.(8)

Overall, influenza is probably most problematic year to year for blood group AB. In general, they are more sensitive to infection by both influenza A and B than the other blood groups. They are affected by these viruses earlier and more severely than those with the other blood groups.

Research shows is that all blood groups will have similar seroconversion frequencies to both the live attenuated and killed subunit vaccines after the administration of two doses. But after only one dose of the live vaccine, blood group A is much more likely than the other blood groups to seroconvert. so must be given by inhalation. Its use might also be limited by its cost. So far, researchers claim that resistance of the virus to the drug has been only rarely observed (but remains a possible area of concern).(9)

Abstracts

References

Polymorphism of human blood groups and incidence of influenza A/Hong Kong (H3N2)

Acta Virol. 1975 Sep;19(5):406-12. Frolov VK, Sokhin AA, Sotnik AY, Frolov AK, Lebedinsky AP, Potapova NA, Lapina LM.

  • During three epidemics of influenza A/Hong Kong (H3N2) and experimentally in vaccines, the relation between influenza infection and ABo, Rh and MN blood groups was studied. Examinations of 2760 patients with laboratory-confirmed diagnosis of influenza and 749 persons vaccinated with live influenza vaccine showed that individuals of blood groups O and B were susceptible to influenza 1.67 and 1.20 times more, respectively, than individuals of blood group A. The difference in incidence was most manifested in first attacks and decreased in subsequent epidemics. The increased incidence in individuals of blood groups O and B as compared to those of blood group A was not associated with factors of specific (antibody) and nonspecific (interferon) resistance to influenza but was related to a greater capacity of leukocytes from these individuals to adsorb the virus. No relation between blood groups Ph and MN and incidence of influenza A/Hong Kong (H3N2) was established.

References

Inhibitory activity of blood group antigens M and N in inhibition of virus influenza hemagglutination

Med Pregl. 2000 Jan-Feb;53(1-2):7-14.

Vojvodic S.

  • RESULTS: Reactivity of erythrocytes with MM and NN phenotypes in titration of hemagglutinins of influenza virus A2 Singapore in which base is viral hemagglutination is identical, because there are no statistically significant differences of average geomaterical levels of antibody titers. Enzymatically derived red cells by papain, which do not contain M and N blood group antigens, not cause viral hemagglutination phenomenon, because they sediment in all dilutions. Reactivity of red blood cells with MM and NN phenotypes in retitration of haemagglutinins and inhibition reaction of hemagglutination is identical, because there are no statistically significant differences in results with two kinds red blood cells. DISCUSSION: Results of investigation revealed that the reactivity of O human red blood cells different in MN phenotype is identical in regard to speed of reaction and receptor capacity in titration, retitration and inhibition reaction of viral hemagglutinatination and also showed that they demonstrate viral hemagglutination phenomenon in contrast with papainised red blood cells which do not contain M and N blood group antigens, which indirectly means that M and N blood group antigens contain receptors for influenza virus. CONCLUSIONS: Human red cells with MM and NN phenotypes cause viral hemagglutination phenomenon with influenza virus A2 Singapore, and could be used in routine virusological diagnostic procedures. O blood group red cells (MM and NN) in reaction of viral hemagglutination result identically in view of speed of reaction and receptor capacity, and have the same impact on result of this reaction. Enzymatically derived red cells by papain do not cause viral hemagglutination phenomenon, because they do not contain receptors for viral hemagglutinin on red cell membrane surface, which are hydrolazed by papain. Receptors for influenza virus on red cell membrane surface are a component part of M and N blood group antigens which are destroyed by papain.

PMID: 10953546

References

Association between secretor status and respiratory viral illness

Raza MW, Blackwell CC, Molyneaux P, James VS, Ogilvie MM, Inglis JM, Weir DM.

BMJ. 1991 Oct 5;303(6806):815-8.

  • OBJECTIVE--To determine whether non-secretion of blood group antigens is associated with respiratory virus diseases. DESIGN--Study of secretor status in patients with respiratory virus diseases determined by an enzyme linked immunosorbent assay (ELISA) developed to identify Lewis (Le) blood group antigen phenotypes (Le(a) non-secretor; Le(b) secretor). SUBJECTS--Patients aged 1 month to 90 years in hospital with respiratory virus diseases (584 nasal specimens). MAIN OUTCOME MEASURES--Criteria for validation of ELISA (congruence between results on ELISA testing of 1155 saliva samples from a previous study and previously established results on haemagglutination inhibition (HAI) testing, proportions of Le(a), Le(b), and Le- phenotypes in 872 samples of nasal washings from a previous study compared with the normal population). Secretor status of patients determined by ELISA and viruses isolated. RESULTS--Agreement between HAI and ELISA for 1155 saliva samples was 97%. Lewis antigens were detected by ELISA in 854 (97.9%) of nasal washings (Le(a) 233 (26.7%), Le(b) 621 (71.2%), and Le- 18 (2.1%)) in proportions predicted for a northern European population. Secretors were significantly overrepresented among patients from whom influenza viruses A and B (55/64, 86%; p less than 0.025), rhinoviruses (63/72, 88%; p less than 0.01), respiratory syncytial virus (97/109, 89%; p less than 0.0005), and echoviruses (44/44, p less than 0.0005) had been isolated compared with the distribution of secretors in the local population. CONCLUSION--Secretion of blood group antigens is associated with respiratory virus diseases.

Links

References


1. Mackenzie JS, Wetherall JD, Fimmel PJ, et al. Host factors and susceptibility to influenza A infection: the effect of ABO blood groups and HL-A antigens. Dev Biol Stand 1977 Jun 1-3;39:355-62

2. Naikhin AN, Katorgina LG, Tsaritsyna IM, et al. Indicators of collective immunity to influenza depending on the blood group and sex of the population. Vopr Virusol 1989 Jul-Aug;34(4):419-23

3. Aho K, Pyhala R, Visakorpi R. ABO associated genetic determinant in H1N1 influenza. Tissue Antigens 1980 Oct;16(4):310-3

4. Fedorova GI, Slepushkin AN, Popova NS, et al. Correlations of the antigenic specificity of human blood with the levels of antihemagglutinins to influenza viruses. Vopr Virusol 1983 Jan-Feb;28(1):54-7

5. Frolov VK, Sokhin AA, Sotnik AY, et al. Polymorphism of human blood groups and incidence of influenza A/Hong Kong (H3N2). Acta Virol 1975 Sep;19(5):406-12

6. Sominina AA, Tsubalova LM, Karpova LS, et al. Genetic predisposition to latent influenza A virus in children with blood group B(III) as a possible cause of new epidemiologic strains in the countries of South-Eastern Asia. Vestn Ross Akad Med Nauk 1994;(9):21-4

7. Karpova LS, Popova TL, Oleinikova EV, et al. Significance of persons with different blood groups in the influenza type A epidemic process. Zh Mikrobiol Epidemiol Immunobiol 1982;(11):86-91

8. Lebiush M, Rannon L, Kark JD. The relationship between epidemic influenza (A(H1N1) and ABO blood group. J Hyg (Lond) 1981 Aug;87(1):139-46

9. Mackenzie JS, Fimmel PJ. The effect of ABO blood groups on the incidence of epidemic influenza and on the response to live attenuated and detergent split influenza virus vaccines. J Hyg (Lond) 1978 Feb;80(1):21-30