AIM:To evaluate the level of sperm chromosome aberrationsin male patients with hepatitis B,and to directly detectwhether there are HBV DNA integrations in spermchromosomes of hepatitis B patients.METHODS:Sperm chromosomes of 14 tested subjects(5healthy controls,9 patients with HBV infection,including 1with acute hepatitis B,2 with chronic active hepatitis B,4with chronic persistent hepatitis B,2 chronic HBsAg carrierswith no clinical symptoms)were prepared using interspecificin vitro fertilization between zona-free golden hamster ovaand human spermatozoa,and the frequencies of aberrationspermatozoa were compared between subjects of HBVinfection and controls.Fluorescence in situ hybridization(FISH)to sperm chromosome spreads was carried out withbiotin-labeled full length HBV DNA probe to detect the specificHBV DNA sequences in the sperm chromosomes.RESULTS:The total frequency of sperm chromosomeaberrations in HBV infection group(14.8 %,33/223)wassignificantly higher than that in the control group(4.3 %,5/116).Moreover,the sperm chromosomes in HBV infectionpatients commonly presented stickiness,clumping,failureto staining,etc,which would affect the analysis of spermchromosomes.Specific fluorescent signal spots for HBV DNAwere seen in sperm chromosomes of one patient with chronicpersistent hepatitis.In 9(9/42)sperm chromosomecomplements containing fluorescent signal spots,onepresented 5 obvious FISH spots,others presented 2 to 4signals.There was significant difference of fluorescenceintensity among the signal spots.The distribution of signalsites among chromosomes was random.CONCLUSION:HBV infection can bring about mutageniceffects on sperm chromosomes.Integrations of viral DNAinto sperm chromosomes which are multisites and nonspecific,can further increase the instability of spermchromosomes.This study suggested that HBV infection cancreate extensively hereditary effects by alteration geneticconstituent and/or induction chromosome aberrations,aswell as the possibility of vertical transmission of HBV via thegerm line to the next generation. AIM: To evaluate the level of sperm chromosome aberrationsin male patients with hepatitis B, and to directly detectwhether there are HBV DNA integrations in spermchromosomes of hepatitis B patients. METHODS: Sperm chromosomes of 14 tested subjects (5 heyy controls, 9 patients with HBV infection, including 1 with acute hepatitis B, 2 with chronic active hepatitis B, 2 chronic HBsAg carriers with no clinical symptoms) were prepared using interspecific in vitro fertilization between zona-free golden hamster ova and human spermatozoa, and the frequencies of aberrations permatozoa were compared between subjects of HBVinfection and controls. Fluorescence in situ hybridization (FISH) to sperm chromosome spreads was carried out with biotin-labeled full length HBV DNA probe to detect the specific HBV DNA sequences in the sperm chromosomes.RESULTS: The total frequency of sperm chromosome assays in HBV infection group (14.8%, 33/223) wassignificantly higher than that in the con trol group (4.3%, 5/116). Moreover, the sperm chromosomes in HBV infectionpatients commonly presented stickiness, clumping, failureto staining, etc, which would affect the analysis of spermchromosomes. Specific fluorescent signal spots for HBV DNAwere seen in sperm chromosomes of one patient with chronicpersistent hepatitis. 9 (9/42) sperm chromosomecomplements containing fluorescent signal spots, onepresented 5 obvious FISH spots, others presented 2 to 4signals.There was significant difference of fluorescence intensity among the signal spots. the distribution of signalsites among chromosomes was random.CONCLUSION: HBV infection can bring about mutageniceffects on sperm chromosomes.Integrations of viral DNA into sperm chromosomes which are multisites and nonspecific, can further increase the instability of spermchromosomes.This study suggests that HBV infection cancreate extensively hereditary effects by alteration geneticconstituent and / or induction chromosome aberrations, aswell as the possibilityof vertical transmission of HBV via the germ line to the next generation.