THE STATE OF CELL MEDIATED IMMUNITY AMONG HEPATITIS B SURFACE ,ANTGENI CARRIERS IN IRAN,

Abstract

Cell-mediated immune (CMI) s t a t us and sub- popul at i ons o f pe r ipheral b l ood lymphocytes were investigated in one hundre d volunt a ry blood donors who were car r ier s of Ag • HE S A signi f i c ant decr e ase of t otal T-cells observed in HB Ag carri e rs as compared t o normal controls. The percenS t age o f active T-cells a nd B-lymphocytes did not d i f f e r signi f icant ly between the t wo groups .
Addi t ion of aut ologous serum from HE Ag c a r r iers t o s t heir l ymphocyt e s reduced the numbe r of detectabl e cells in HE Ag carriers . This reduction coul d be due to the s presence of a r osette i nhi bitory f actor in their serum. Our studies demonstrated a failur e o f CMI among HB Ags car r i ers detected by the l e ukocyte migr ation i nhibition (LMI) test. This failure cannot be attributed to the presence of HE Ag-AB complexes in their serum. It is s possible that specific failure of CMI allows the hepatitis B virus to remain harmless in carriers a Hepatitis B surface-antigen (HE Ag); Hepatitis Bs coreantigen (HE Ag) and Hepatitis Be-antigen (HE Ag), c e have been established as indicating ineffectivity in viral hepatitis B ({I, 6 , 20, 28).
A number of infected individuals also developed clini cal evidence of disease and HE Ag may s the serum of some subjects for a long rema•ln present I•n time (18). It has been suggested that to a defect in CMI, the persistence of HB Ag s whether liver disease is is related present or not, and impairment of the lymphocyte response to phytohaemagglutinin (PHA) in this group is presented in evide•
nee (8, •9 , 13, 24, 25) .In contrast, other workers report a normal respons e t o PHA in healthy carriers of HE Ag and s they concludE that the defective T-cell response is relat ed to the live!' disease rather than the immune system (31). Dudley et al (8) have suggested that liver damage occurring after hepatitis B infection, may be an effect of thymus-dependent lymphocytes (12).
A variety of in-vitro tests have been employed to demonstrate the status of cellular immunity (30, 35). Amongst these the inhibition of leukocyte migration by different specific and non-specific antigens appears to be a sensitive and convenient procedure (37). Leukocyte Inhibitory Factor (LIF) production in the presence of the virus itself has already been demonstrated Ill) .In a preliminary study lto et al. (14) reported that migration of leukocytes could be inhibited by serum containingHB .Ag. Frei et al. (11) have also reported the effect of s purified, partially purfied and non purified HB Ag ons lymphocytes in acute cases of hepatitis B using the leukocyte migration inhibition test.
The prevalence of HBsAg among some 200,000 voluntary blood donors in Iran was found to be 3.5%(10). We have evaluated the subpopulations of T and B lymphocytes in HB Ag carriers and applied the LMI test in the presence s of PHA, purified protein. derivative (PPD) , crude HB~g positive serum and purified HB~g, in order to define CMI in HS r.q ~ . ~ carr•lers.