Many of these patients with lower CD4 cell counts had experienced prior AIDS-defining events because of late diagnosis of HIV infection [34], and one of them was even receiving acute therapy for toxoplasma encephalitis at the time of the influenza A H1N1 diagnosis. Although some HIV-positive patients

were profoundly immune-suppressed because LDK378 purchase of recent late presentation or incomplete CD4 cell recovery [35–38], we did not find that influenza A H1N1 caused illness preferentially in these patients; nor did these patients show more severe infection. Active smoking and former/current injecting drug use, but not the degree of immunosuppression, as indicated by CD4 cell counts, were risk factors for pneumonia in HIV-positive patients with influenza A H1N1 infection. Injecting drug use [39,40] and tobacco smoking [41] are widely recognized risk factors for bacterial pneumonia in HIV-infected patients. Of note, three (60%) of the five HIV-positive patients with confirmed influenza A H1N1 infection presenting with pneumonia

had concomitant infection with Streptococcus pneumoniae detected. We found that a longer time from the onset of symptoms to hospital admission was independently associated with a more severe presentation, such as pneumonia, in this group of patients as a whole. A later diagnosis may lead to a delay in the initiation of specific anti-influenza selleck products therapy. Investigators from Mexico City reported that, in a series of severely immune-suppressed

HIV-infected adults who were receiving care for underlying opportunistic respiratory infections, including Pneumocystis pneumonia and tuberculosis, a concomitant diagnosis of influenza A H1N1 infection was not initially suspected [42]. Of 27 HIV-positive patients with influenza A H1N1 infection seen during the initial months of the Mexico City epidemic, 14 required hospitalization and six died. In addition, there are anecdotal reports 3-mercaptopyruvate sulfurtransferase of HIV-infected patients with severe or fatal influenza A H1N1 infection [43,44]. These cases indicate that influenza A H1N1 infection can be severe in already severely ill HIV-positive patients presenting with concomitant opportunistic infections; in these patients, the missed diagnosis of influenza H1N1 and the subsequent delay in the provision of specific anti-influenza therapy may be fatal. However, our study and others [45,46] suggest that HIV-positive adults are generally no more likely to experience severe complications of H1N1 influenza virus infection than adults not infected with HIV. Similar to seasonal influenza [47], we confirmed that influenza A H1N1 infection did not adversely affect surrogate markers such as CD4 and CD8 cell counts and HIV-1 RNA in plasma or HIV disease progression. Our study had several limitations. HIV-negative controls were assumed to be HIV-uninfected, but we did not confirm this.