In most of the earlier reports on H5N1 cases, the number of cases was not large enough to adjust for potential confounders. However, several published studies did investigate factors that predicted poor outcome, adjusting the confounders for the whole-age spectrum of the subjects. Kandun et al. [12] analyzed 127 confirmed infections from June 2005 through February 2008 in Indonesia and found that an individual case was significantly associated with the mortality. Liem et al. [13] reviewed medical records and analyzed 67 of 93 cases of H5N1 infection in Vietnam from January 2004 through December 2006. Applying a backward step-wise variable selection strategy for logistic regression analysis, these researchers were able to show that the presence of both neutropenia and raised ALT level predicted a poor outcome. Yu et al. [14] collected 26 H5N1 cases from hospital medical records of H5N1 cases in China from October 2005 through April 2008 and found that decreased PLT count, elevated lactic dehydrogenase level, ARDS, and cardiac failure were associated with mortality. In our study, decreased WBC and PLT counts were significantly associated with the prognosis adjusted with sex and age, but these results coincided with the results of individual previous reports. Both decreased WBC and PLT counts are considered to be common predictors of poor prognosis in H5N1 influenza patients \18 years of age. Further studies that include larger numbers of patients are needed to clarify these results.  Human monoclonal IgG selection of Plasmodium falciparum for the expression of placental malaria-specific variant surface antigens Pregnancy-associatedPlasmodium falciparum malaria (PAM) is a major cause of morbidity and mortality in African women and their offspring. PAM is characterized by accumulation of infected erythrocytes (IEs) that adhere to chondroitin sulphate A (CSA) in the placental intervillous space. We show here that human monoclonal IgG antibodies with specificity for variant surface antigens (VSA) specifically expressed by CSA-adhering IEs (VSA(PAM)) can be used in vitro to select parasites from nonpregnant donors to express VSA(PAM) and that this selection for VSA(PAM) expression results in preferential transcription of var2csa. The results corroborate current efforts to develop PAM-specific vaccines based on VAR2CSA. Children living in areas of stable Plasmodium falciparum transmission acquire substantial protective immunity against malaria during the first decade of life. Protection is mediated to a large extent by variant surface antigen (VSA)specific IgG. Nevertheless, women in such areas remain highly susceptible to P. falciparum infection if they become pregnant, as the parasites can switch to expression of particular VSA (called VSA PAM ), which allow infected erythrocyte (IE) sequestration in the placenta, but which are not compatible with parasite survival in a nonpregnant host. Acquired immunity to PAM is mediated by VSA PAMspecific IgG that either opsonizes IEs for phagocytosis or interferes with chondroitin sulphate A (CSA)-specific adhesion of IEs (1) . VAR2CSA, which is a member of the P. falciparum erythrocyte membrane protein 1 (PfEMP1) family of VSA, appears to be the dominant or only pregnancy-associated Plasmodium falciparum malaria (PAM) type VSA in the P. falciparum genome, and is therefore the main target of current efforts to develop a vaccine against PAM (2) . To assist this work, we have developed a panel of VSA PAM -specific human IgG1 monoclonal antibodies (3) , which can opsonize VSA PAMexpressing IEs for phagocytosis and interfere with IE adhesion to CSA (Barfod et al . unpublished data) . These antibodies can be used to enrich for VSA PAM expression in parasites not expressing VSA PAM but obtained from women with PAM (3) . In the present study we used two of the above-mentioned monoclonal antibodies to select for VSA PAM expression in parasites from nonpregnant donors. One antibody (PAM1·4) was chosen because it appears to react with most or all parasites expressing VSA PAM . The other antibody (PAM8·1) was chosen because it reacts with a well-defined, but inter-clonally variant, epitope in the DBL3X domain of VAR2CSA.