***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: We describe the aetiology of community-acquired pneumonia ( CAP ) in HIV-infected patients , risk factors for bacterial or Pneumocystis jirovecii CAP and prognostic factors of 30-day mortality . This was a prospect i ve observational study of 331 consecutive adult CAP cases in HIV-infected patients ( January 2007 to July 2012 ) . 128 ( 39 % ) patients had CD4 + cell counts < 200 per mm3 and 99 ( 43 % ) ha HIV RNA levels < 200 copies per mL on antiretroviral therapy . Streptococcus pneumoniae was the most frequent microorganism in the group with CD4 + cell counts ≥200 per mm3 ; P. jirovecii was the most frequent microorganism in the group with CD4 + cell counts < 200 per mm3 and in patients with HIV RNA ≥200 copies per mL. Predictors of bacterial CAP were : time with symptoms ≤5 days ( OR 2.6 , 95 % CI 1.5–4.4 ) , C-reactive protein level ≥22 mg·dL−1 ( OR 4.3 , 95 % CI 2.3–8.2 ) and hepatitis C virus co-infection ( OR 2.3 , 95 % CI 1.4–3.9 ) . White blood cell count ≤4 × 1012 per L ( OR 3.7 , 95 % CI 1.2–11.5 ) , lactate dehydrogenase ( LDH ) level ≥598 U·L−1 ( OR 12.9 , 95 % CI 4.2–39.7 ) and multilobar infiltration ( OR 5.8 , 95 % CI 1.9–19.5 ) were predictors of P. jirovecii . Overall 30-day mortality was 7 % .  Appropriate antibiotic treatment ( OR 0.1 , 95 % CI 0.03–0.4 ) , LDH ≥598 U·L−1 ( OR 6.2 , 95 % CI 1.8–21.8 ) and mechanical ventilation ( OR 22.0 , 95 % CI 6.2–78.6 ) were the variables independently associated with 30-day mortality . The described predictors may help clinicians to distinguish between bacterial and P. jirovecii pneumonia in patients with suspected or confirmed HIV infection . Clinical risk factors in HIV patients to distinguish between bacterial and Pneumocystis jirovecii pneumonia Rationale : Human immunodeficiency virus ( HIV ) infection is associated with pulmonary disease and worse lung function , but the relationship of lung function with survival in HIV is unknown . Objectives : To determine whether lung function is associated with all‐cause  mortality in HIV‐infected individuals . Methods : HIV‐infected participants from cohorts in three locations underwent pre‐ and post‐bronchodilator spirometry and determination of single‐breath diffusing capacity of the lung for carbon monoxide ( DlCO ) in 2008‐2009 , computed tomographic ( CT ) scanning of the chest for quantitative emphysema and airway measures , and echocardiography for estimated left ventricular systolic and diastolic function and tricuspid regurgitant velocity . Bivariate analysis and multivariable Cox proportional hazards models were used to determine whether decreased lung function was independently associated with increased all‐cause mortality . Models were adjusted for covariates including age , sex , body mass index , smoking status , self‐reported hepatitis C status , HIV viral levels , CD4 + T‐cell counts , hemoglobin , antiretroviral therapy , and illicit drug use . Results : Overall , 396 HIV‐infected participants underwent pulmonary function testing . Thirty‐two participants ( 8 % ) died during a median follow‐up period of 69 months . A post‐bronchodilator FEV1‐to‐FVC ratio less than 0.7 ( hazard ratio [ HR ] , 2.47 ; 95 % confidence interval [ CI ] , 1.10‐5.58 ) and a DlCO less than 60 % ( HR , 2.28 ; 95 % CI , 1.08‐4.82 ) were independently associated with worse mortality . Also , hepatitis C ( HR , 2.68 ; 95 % CI , 1.22‐5.89 ) and baseline plasma HIV RNA level ( HR per ln RNA copies/ml , 1.50 ; 95 % CI , 1.22‐1.86 ) were associated with mortality in HIV‐infected participants . The only CT or echocardiographic measure associated with greater mortality in univariate analysis was greater wall thickness of medium‐sized airways ( HR for wall area percent , 1.08 ; 95 % CI , 1.00‐1.18 ; P = 0.051 ) , but none of the CT or echocardiogram measures were associated with mortality in multivariable analysis . Conclusions : Airflow obstruction and impaired diffusing capacity appear to be associated with all‐cause mortality in HIV‐infected persons over an average of 6 years of follow‐up . These data highlight the importance of lung dysfunction in HIV‐infected persons and should be confirmed in larger cohorts and with extended follow‐up periods . Clinical trial registered with www . clinical trials.gov ( NCT00869544 , NCT01326572 ) The aim of our study was to analyse the impact of time from onset of symptoms on the systemic cytokine concentrations in patients with pneumococcal pneumonia . Adults with severe pneumococcal pneumonia were prospect ively included . At admission , vital signs , time from onset of pneumonia symptoms and circulating levels of C-reactive protein ( CRP ) , serum amyloid A ( SAA ) , tumour necrosis factor (TNF)-α , and interleukin (IL)-1β , IL-6 , IL-8 , IL-10 and IL-1ra were recorded . 32 patients were included ; 13 patients had < 48 h of evolution and 19 patients had been sick for > 48 h. The group with a longer time of evolution presented higher plasmatic levels of TNF-α ( 19.1±8.5 versus 35.5±26 pg·mL−1 ) , fibrinogen ( 6±1.8 versus 9±2 ) ; CRP ( 130±85 versus 327±131 ) and SAA ( 678±509 versus 984±391 ) . Concentrations of TNF-α were associated with the presence of bacteraemia , initial blood pressure < 90 mmHg and with a lower oxygen saturation at admission . Likewise , TNF-α levels were correlated with concentrations of IL-1β ( r = 0.49 ) , IL-6 ( r = 0.41 ) and IL-8 ( r = 0.40 ) . In pneumococcal pneumonia , patients with a longer time of evolution presented with higher levels of pro-inflammatory cytokines and a higher expression of acute phase proteins , suggesting a sustained release of pneumococcal antigens over time BACKGROUND Observational data have been conflicted regarding the potential role of HIV antiretroviral therapy ( ART ) as a causative factor for , or protective factor against , COPD . We therefore aim ed to investigate the effect of immediate versus deferred ART on decline in lung function in HIV-positive individuals . METHODS We did a nested sub study within the r and omised , controlled Strategic Timing of Antiretroviral Treatment ( START ) trial at 80 sites in multiple setting s in 20 high-income and low-to-middle-income countries . Participants were HIV-1 infected individuals aged at least 25 years , naive to ART , with CD4 T-cell counts of more than 500 per μL , not receiving treatment for asthma , and without recent respiratory infections ( baseline COPD was not an exclusion criterion ) . Participants were r and omly assigned to receive ART ( an approved drug combination derived from US Department of Health and Human Services guidelines ) either immediately , or deferred until CD4 T-cell counts decreased to 350 per μL or AIDS developed . The r and omisation was determined by participation in the parent START study , and was not specific to the sub study . Because of the nature of our study , site investigators and participants were not masked to the treatment group assignment ; however , the assessors who review ed the outcomes were masked to the treatment group . The primary outcome was the annual rate of decline in lung function , expressed as the FEV1 slope in mL/year ; spirometry was done annually during follow-up for up to 5 years . We analysed data on an intention-to-treat basis , and planned separate analyses in smokers and non-smokers because of the known effects of smoking on FEV1 decline . The sub study was registered at Clinical Trials.gov number NCT01797367 . FINDINGS Between March 11 , 2010 , and Aug 23 , 2013 , we enrolled 1026 participants to our sub study , who were then r and omly assigned to either immediate ( n=518 ) or deferred ( n=508 ) ART . Median baseline characteristics included age 36 years ( IQR 30 - 44 ) , CD4 T-cell count 648 per μL ( 583 - 767 ) , and HIV plasma viral load 4·2 log10 copies per mL ( 3·5 - 4·7 ) . 29 % were female and 28 % were current smokers . Median follow-up time was 2·0 years ( IQR 1·9 - 3·0 ) . We noted no differences in FEV1 slopes between the immediate and deferred ART groups either in smokers ( difference of -3·3 mL/year , 95 % CI -38·8 to 32·2 ; p=0·86 ) or in non-smokers ( difference of -5·6 mL/year , -29·4 to 18·3 ; p=0·65 ) or in pooled analyses adjusted for smoking status at each study visit ( difference of -5·2 mL/year , -25·1 to 14·6 ; p=0·61 ) . INTERPRETATION The timing of ART initiation has no major short-term effect on rate of lung function decline in HIV-positive individuals who are naive to ART , with CD4 T-cell counts of more than 500 per μL. In light of up date d WHO recommendations that all HIV-positive individuals should be treated with ART , regardless of their CD4 T-cell count , our results suggest an absence of significant pulmonary harm with such an approach . FUNDING US National Heart Lung and Blood Institute , US National Institute of Allergy and Infectious Diseases , Division of AIDS , Agence Nationale de Recherches sur le SIDA et les Hipatites Virales ( France ) , Australian National Health and Medical Research Council , Danish National Research Foundation , European AIDS Treatment Network , German Ministry of Education and Research , UK Medical Research Council and National Institute for Health Research , and US Veterans Health Administration Office of Research and Development Human immunodeficiency virus (HIV)-associated respiratory infections , most notably Pneumocystis carinii pneumonia ( PCP ) , but also bacterial pneumonia ( BP ) , result in reductions in lung function that have been studied mainly during the course of acute infection . Whether HIV-associated pneumonias also cause permanent changes in pulmonary function is unknown . In this study we investigated the long-term effects of PCP and BP on pulmonary function in a cohort of HIV-infected persons . One thous and , one hundred forty-nine HIV-infected persons were followed in a prospect i ve , observational cohort study at six centers in the United States . Study participants had pulmonary function testing performed at regular preset intervals . PCP and BP diagnoses were verified with defined criteria . Longitudinal multivariate analysis was used to model pulmonary function in terms of demographic data and occurrence of PCP or BP . We found that PCP or BP was associated with permanent decreases in FEV(1 ) , FVC , FEV(1)/FVC , and the diffusing capacity of carbon monoxide . Neither infection result ed in statistically significant changes in TLC . We conclude that PCP and BP result in expiratory airflow reductions that persist after the acute infection resolves . The clinical implication s of these changes are unknown , but they may contribute to prolonged respiratory complaints in HIV-infected patients who have had pneumonia Background HIV-infected individuals have increased risk of developing obstructive lung disease ( OLD ) . Studies from developed countries report high viral load , low CD4 counts , and anti-retroviral therapy ( ART ) to be associated with OLD ; but these findings may not be generalizable to population s in re source -limited setting s. Methods We conducted a prospect i ve cohort study of lung function in 730 HIV-infected black South African adults .  Pre-bronchodilator spirometry was performed at enrollment and repeated annually for three years . Logistic regression models were used to identify factors associated with OLD , defined as FEV1/FVC<0.70 , at enrollment . Excess annual declines in FEV1 and FVC were modelled as the product-term of follow-up time and exposures using r and om effects regression . Results Median ( IQR ) age at enrollment was 36 ( 32–41 ) years , 85 % were female and 30 % ever-smoked with a median ( IQ 
    Output:
    
Markers of inflammation ( IL-6 , TNF-α , CRP ) , innate defense ( cathelicidin ) , monocyte and macrophage activation ( sCD14 , sCD163 and , IL-2sRα ) , endothelial dysfunction ( ET-1 ) and general immune health ( CD4/CD8 ratio ) were associated with lung abnormalities in HIV .