Differences between laboratory data at hospital admission between fatal and nonfatal cases are shown in Table 3 . Leukopenia and thrombocytopenia at hospital admission were present in the fatal cases, but there were no differences in the serum levels of AST and ALT between fatal and nonfatal cases. In the linear regression analysis performed to investigate the association between blood cell counts and prognosis, WBC and PLT were dependent variables, and age, sex, and prognosis were independent variables. In the linear regression analysis performed to investigate the association between log-transformed liver function data and prognosis, log AST and log ALT levels were dependent variables, and age and prognosis were independent variables as the sample size was small enough to enable one covariate to be added. Standardized regression coefficients for the results of these linear regression analyses are shown in Table 4 . Death (the value of prognosis = 1) was negatively associated with WBC and PLT counts adjusted with age and sex. In contrast, increased log AST tended to be associated with poor prognosis, but there was no significant association between survival and log [1] with the results from the pooled data of our five studies reveals that the CFR for patients\19 years of age was 56.9% in the WHO report and 69.4% in our pooled data. The median time from onset of symptoms to admission was 4 days (mean 4.6 days) among all of the patients reported in our five studies and 5 days in patients reported to have died in the WHO report. The median time from onset to admission was 6 days in the pooled data. Cases were mainly identified through passive surveillance in the WHO report, whereas we also included cases collected through hospital medical records in our study. Thus, the CFR in the pooled data was higher than that of the WHO report, and the median time from onset to admission in the pooled data was longer than that in the WHO report. Our pooled data was biased to include more severe cases. Significant variations in patterns that may reflect differences in exposure related to social behavior, cultural and religious practices, access to care, and treatment or virulence of the viruses among countries have been pointed out in previous reports [4] . With respect to the virulence of viruses, viruses capable of infecting humans have been divided into groups from clades and subclades 0, 1, 2.1, 2.2, 2.3, and 7 from the phylogenetic tree for the hemagglutinin gene of highly pathogenic avian influenza A (H5N1) viruses. Clade 1 viruses were found to predominate in Vietnam, Thailand, and Cambodia in the early phase of the outbreak (2004) (2005) , and clade 2.1 viruses are endemic in Indonesia (2005) (2006) . Clade 2.2 viruses were associated with the outbreak of avian infection in Central and South Asia, the Middle East, Europe, and Africa and with human infection in western Asia, the Middle East, and Africa (including the Turkish outbreak from 2005 to 2006). The median time from onset to hospitalization were found to be unchanged among clades [11] . Differences in the proportion of fatalities were observed, but it is difficult to determine whether this difference was due to the difference in viral virulence, as other variations existed among countries.