CMV Co-infection Research Articles

Preserved immune functionality and high CMV-specific T-cell responses in HIV-infected individuals with poor CD4+ T-cell immune recovery

Poor CD4+ T-cell recovery after cART has been associated with skewed T-cell maturation, inflammation and immunosenescence; however, T-cell functionality in those individuals has not been fully characterized. In the present study, we assessed T-cell function by assessing cytokine production after polyclonal, CMV and HIV stimulations of T-cells from ART-suppressed HIV-infected individuals with CD4+ T-cell counts >350 cells/μL (immunoconcordants) or <350 cells/μL (immunodiscordants). A group of HIV-uninfected individuals were also included as controls. Since CMV co-infection significantly affected T-cell maturation and polyfunctionality, only CMV+ individuals were analyzed. Despite their reduced and skewed CD4+ T-cell compartment, immunodiscordant individuals showed preserved polyclonal and HIV-specific responses. However, CMV response in immunodiscordant participants was significantly different from immunoconcordant or HIV-seronegative individuals. In immunodiscordant subjects, the magnitude of IFN-γ+ CD8+ and IL-2+ CD4+ T-cells in response to CMV was higher and differently associated with the CD4+ T-cell maturation profile., showing an increased frequency of naïve, central memory and EMRA CMV-specific CD4+ T-cells. In conclusion, CD4+ and CD8+ T-cell polyfunctionality was not reduced in immunodiscordant individuals, although heightened CMV-specific immune responses, likely related to subclinical CMV reactivations, may be contributing to the skewed T-cell maturation and the higher risk of clinical progression observed in those individuals.

Prevalence of Human Cytomegalovirus Infection among Human Immunodeficiency Virus Positive Women Receiving Antiretroviral Treatment at Federal Teaching Hospital Abakaliki, Ebonyi State, Nigeria

Background: Cytomegalovirus has been identified as the major cause of morbidity and mortality among neonates. It commonly occurs in immunocompromised and immunodepressed individuals. Objectives: This study was conducted to determine the occurrence of CMV infection amongst HIV-positive women receiving antiretroviral treatment at Federal Teaching Hospital Abakaliki (FETHA). Socio-demographic factors associated with CMV and HIV were also examined. The population of volunteers present for the study was 124 Persons. Study Design: Blood samples were collected from the study subjects and recent infection of CMV was investigated using the Enzyme Linked Immunosorbent Assay ELISA), which detects Immunoglobulin M (IgM). Results: The result obtained indicated that 14 (11.3%) out of the 124 already confirmed HIV patients had recent/current CMV infection. Again, 18 of the patients were either pregnant or within two weeks of delivery, among which 3 (16.7%) were CMV positive. The study also showed that CMV and HIV co-infection predominates among the age group 26-30 years (15.6%), singles (13.9%), and unemployed (15.8%) of the tested population. The level of education had no effect on the rate of co-infection of CMV and HIV. Conclusion: This study shows the rate of infection and reactivation of CMV among HIV positive patients receiving antiretroviral treatment at Federal Teaching Hospital Abakaliki, Ebonyi State, Nigeria. CMV infection predominates among the Single HIV-positive individuals, within the age group 26-30 years, followed by Civil Servants and the unemployed. We therefore recommend that serious and aggressive campaign be carried out in this region and elsewhere where CMV and HIV co-infection is endemic or prevalent in order to curtail the transmission of the disease and thus reduce the possible menace posed by this virus.

Co-Colitis: A Rare Case of C. difficile and CMV Coinfection in an IBD Patient

Co-Colitis: A Rare Case of C. difficile and CMV Coinfection in an IBD Patient

Outcome of renal transplant recipients with CMV and BKV co-infection nephropathy

Outcome of renal transplant recipients with CMV and BKV co-infection nephropathy

Immunopathology of CMV Co-Infection: Review

CMV is a common complex viral infection that affects patients at all ages, especially newborns. It causes a lifelong infection with a frequency of approximately 80% of the population will become infected by age 40. Most CMV infection is silent infection (no symptoms), however, in immunocompromised individuals, a symptomatic infection persists with few medical treatments or vaccine currently available. Coinfection of CMV with other viruses had drawn much attention in the last decade, as diagnostic methodologies became more reliable, and many cases have been reported. The long-term relationships between immune responses, viral load, and most importantly, disease progression in those who are persistently infected with CMV are still poorly understood. This review will summarize the current knowledge of the immunopathological features of different CMV co-infections and highlight the importance of considering CMV co-infection in the patient treatment and management.

Immunopathology of CMV Co-Infection: Review

Immunopathology of CMV Co-Infection: Review

Relative risks for digestive and respiratory episodes in patients with HIV co-infection

HBV, CMV or TB co-infection worsen progression of HIV, due to specific pathogenicity of etiologic agents and antimicrobial therapy which is required to be initiated. Authors have tried to establish a link between HBV, CMV or TB co-infection and the risks for emergence of digestive and respiratory episodes. We have used data from the medical records of HIV-AIDS department of Arad County Emergency Hospital for HIV patients in evidence in 2013. Data were analyzed SPSS.14.0 for Windows, MedCalc and Epi Info Analysis. Of the 149 patients 38 presented HBV, CMV or TB co-infection (25.5%) and statistically was significant in the history of their recorded adverse reactions that changing ART regimens was required (P=0.0324), they also displayed digestive and respiratory episodes P=0.0057 and P=0.0033, being at relative risk of 1.7344 to 1.6692 respectively for these episodes compared with HIV patients co-infection. HIV patients with co-infection stand at increased risk for digestive and respiratory intercurrent infectious episodes, monitoring them being a basic element for their quality of life and for survival rates improvements.

Subclinical Atherosclerosis and Markers of Immune Activation in HIV-Infected Children and Adolescents

HIV-infected adults display increased cardiovascular disease, probably driven by inflammation and immune activation. These relationships have not been addressed in vertically HIV-infected children and adolescents, a population at very high risk for long-term non-AIDS complications. Carotid intima media thickness (IMT) was measured in a cohort of HIV-infected children and adolescents and healthy controls. C-reactive protein and markers of immune activation (CD38⁺HLA-DR⁺) and immune senescence (CD28⁻CD57⁺) were determined. One hundred fifty HIV-infected patients and 150 controls were included, 64.8% female. IMT was thicker in HIV-infected patients (0.434 mm ± 0.025 vs. 0.424 mm ± 0.018, P < 0.001). After adjustment by age, sex, body mass index, and smoking status, HIV infection was independently associated with thicker IMT (odds ratio, 2.28; 95% confidence interval: 1.25 to 4.13; P = 0.007). Among HIV-related variables, a low CD4 nadir was related to an increased IMT. Although HIV-infected subjects presented higher frequencies of activated CD4⁺ and CD8⁺ T cells (P = 0.002 and P = 0.087, respectively), no relation was found between IMT and inflammation, immune activation, or senescence. Structural changes of the vasculature present early in vertically HIV-infected subjects as well as immune activation and senescence. These patients should be carefully monitored for the prompt detection and early treatment of cardiovascular disease.

Controlled Epstein-Barr Virus Reactivation After Allogenic Transplantation Improves Survival and Is Associated To An Expansion Of Natural Killer Cells (NK)

Background B-lymphocytes infected by the Epstein-Barr virus (EBV) are strongly controlled by the immune system, with the persistence of low counts of EBV-infected B lymphocytes in 98% of healthy individuals. Both T- and Natural Killer (NK)-lymphocytes play a main role in immune surveillance of EBV infection. EBV-reactivation (R) frequently occurs in patients having allogeneic transplantation (AT). Aims We evaluated the impact of controlled EBV-R on survival of allografted adult patients with haematological malignancies and analyzed the different circulating lymphocyte populations. Methods 190 consecutive adult patients were included in this study. Patients received fludarabine, busulfan, ATG for reduced intensity conditioning regimen or cyclophosphamide plus TBI for myeloablative conditioning regimen. Prophylaxis of acute GVHD was conventional. EBV viral load (EBV-VL) was monitored in PB, for all the patients after AT, weekly for the first 6 months, then monthly using standard PCR technique. EBV-R was defined by an EBV-VL ³500 copies/ml, increasing 1 week later. This cut-off level of EBV-VL was used to decide therapy, first reducing immunosuppression followed by rituximab if no EBV-VL decrease (375mg/m2, 4 injections weekly). Lymphocyte immunophenotyping (CD3,4,8,3+56+,3-56+,19,25,DR) was performed weekly for 3 months, then monthly using standard technique. In order to show interdependency between the parameters, a multivariate analysis was performed for OS and PFS including parameters like EBV-R, ATG usage. All analysis was performed with SAS 9.3. Results There were 105 acute leukaemias (26 ALL, 71 AML) and myelodysplastic syndromes (8), 71 lymphoproliferative disorders (17 lymphomas, 8 CLL and 46 MM), 5 aplastic anaemia and 9 CML. There were 76 females and 114 males (median age: 51y, range 18-69). 86 (45%) patients presented EBV-R, with 74 patients having EBV-VL&gt;1000 copies/mL. There was no statistical difference between the 2 groups of patients (EBV-R and no EBV-R), for age, sex, cancer type, conditioning regimen, particularly fludarabine, type of graft, and number of infused CD34+ hematopoietic progenitors. Patients with EBV-R received more frequently ATG (P =0.004). The median time of EBV-R detection was 73 days (IQR: 40-210) after transplantation. In case of EBV-R, the dose of immunosuppressive drugs was reduced before stopping. 69/86 patients received rituximab. Patients with no EBV-R did not receive rituximab. Within the 3 months after rituximab, GVHD intensity was decreased, particularly for acute GVHD, which was less frequent. The median follow up was 36.6 months (95%IC 31.5-45.7). Patients with EBV-R had a longer PFS than those with no EBV-R (at 2 years 51% vs. 69%, at 5 years 47% vs 38%) (P&lt;.04). Similarly, OS was longer in patients with EBV-R than that observed for patients with no EBV-R (at 2 years 76% vs. 64% and at 5 years 63 % vs. 47%, P&lt;.001). OS and PFS were not different between patients according to the type of hematological malignancy (respectively, P=.46 and P=.49). The use of ATG was not a significant factor on OS (univariate (p=0.93) and multivariate analysis (p=0.81)). Similarly, it was not a significant factor on PFS (univariate (p=0.47) or multivariate analysis (p=0.68)). Among the patients with EBV-R, OS and PFS were not significantly different for patients receiving or not rituximab (respectively p=0.67 and p=0.88). The median duration of lymphocyte measurement was 94 days (IQR 59-248) after AT. B-lymphocytes and particularly T-lymphocytes, including CD4+ and CD8+ lymphocytes were not significantly different between the 2 groups, respectively P=.29 and P=.48. Only circulating NK cells were significantly different, with a median increased by 22% (P=.03) in patients with EBV-R. CMV co-infection did not impact NK cell counts (P=.058). NK cell count was not different according the use of rituximab (P=.22). The use of rituximab did not modify NK cell counts at 3 and 6 months after stopping treatment (both P=.99). Conclusions Controlled EBV-R in allografted cancer patients is associated with better OS and PFS, in association with a significant increase in circulating NK cells. A prospective study is ongoing for analyzing different subpopulations of NK cells. Disclosures: No relevant conflicts of interest to declare.

Severe Pneumocystis jiroveci Pneumonia in a HIV Patient With Normal CD4 Count - Role of CMV Coinfection?

Severe Pneumocystis jiroveci Pneumonia in a HIV Patient With Normal CD4 Count - Role of CMV Coinfection?

Detection of cytomegalovirus DNA on dried blood spots collected from infants infected with HIV: An in-house method adaptable in resource-limited settings

In countries with limited resources, infants infected with HIV are highly exposed to CMV co-infection which probably represents a major risk factor for disease progression in this population. This study aimed to evaluate the performance of a low cost CMV DNA extraction method from DBS and the feasibility of its implementation in laboratories of 4 countries with limited resources. DNA was extracted from DBS with a cationic resin (chelex 100) and amplified with an “in house” real time CMV PCR. Dilutions of a quantified whole blood sample were spotted on paper to evaluate the 95% detection limit. A DBS quality control panel was analyzed in all laboratories. CMV PCR was compared between DBS and liquid whole blood (gold standard) in 2 populations: 418 transplanted patients and 59 infants infected with HIV (median age of 2 months). The CMV PCR 95% detection limit in DBS was 3.87log10copies/mL. Its positive and negative predictive values for CMV diagnosis in infants infected with HIV were 100% and 87.5% respectively. Quality control panels gave consistent qualitative results in all laboratories. This assay had high predictive values for CMV diagnosis in infants infected with HIV and its implementation in resource-limited countries with limited resources is feasible.

NKG2C+CD57+ CD56dim NK cells are enriched following Epstein-Barr virus transformed lymphoblastoid cell line co-culture with peripheral blood mononuclear cells from cytomegalovirus+ donors (P4359)

Abstract Cytomegalovirus (CMV) is a persistent herpesvirus that promotes NKG2C+ Natural Killer (NK) cell differentiation. Highly mature CD57+ NKG2C+ NK cells have been proposed as the equivalent of mouse memory-like NK cells, which have features as long-term persistence and enhanced recall responses. AIM: To examine if co-infection with another common herpesvirus, Epstein-Barr virus (EBV), affects the NKG2C+ CD56dim NK cell population. METHODS: PBMCs from 45 five-year old children with known EBV and CMV serostatus were phenotyped. Further, PBMCs from 6 CMV sero+ EBV sero- infants were used for co-culture with EBV+ lymphoblastoid cell-lines (LCLs) during 72 hours. EBV- LCLs (Ramos) served as controls. Anti CD3, CD14, CD19, CD56, CD57, NKG2C and ki-67 antibodies were used for flow cytometric analysis. RESULTS: EBV and CMV co-infection was related to higher proportions of NKG2C+ and NKG2C+CD57+ CD56dim NK cells compared to infection with CMV or EBV alone, or seronegativity. In contrast to co-culture with Ramos, PBMC co-culture with EBV+ LCLs generally led to enrichment of NKG2C+CD57+ NK cells (stimulation index median 1.23, range 0.87-1.30), which was not related with higher NK cell proliferation. CONCLUSIONS: EBV co-infection seems to promote the existence of higher proportions of memory-like NK cells. Our data herein indicate that this is not due to enhanced proliferation of these cells; rather it suggests that memory-like NK cells may be maintained by EBV co-infection.

MCMV alters the airway inflammatory milieu regulating protective and pathogenic heterologous immunity to influenza A virus infection (P6137)

Abstract Prior immunity to apparently unrelated pathogens can affect the course of subsequent acute infections. The mechanisms of heterologous regulation in most circumstances remain poorly defined. In mice co-infected with murine cytomegalovirus (mCMV) and Influenza A virus (IAV), we show that prior infection with mCMV results in significantly reduced weight loss upon acute challenge with IAV as well as improved recall responses. Tetramer and ex-vivo ICCS assay showed an early recruitment of mCMV specific CD44hi CD62Llo IFNγ+ TNFα+ CD8 T cells in the bronchoalveolar lavage (BAL) of both acutely and latently infected animals following IAVx31 challenge that was absent in mice infected with CMV-alone. This protection was dependent on IFNγ production by these mature anti-CMV CD8 T cells, the protective phenotype was completely ablated in co-infected IFNγ-/- animals or in animals co-infected simultaneously. However, no cross-reactive T cells were detectible. Furthermore, comparative kinetics of CMV specific CD8 T cell responses showed that IAV infection resulted in the attrition of the CMV specific CD8 T cell response in both acutely and latently infected animals. Finally, analysis of the IAV-specific T cell receptor repertoire by multiplex nested PCR suggested that prior CMV infection altered the recruited IAV-specific T cell repertoire. These data demonstrate that CMV co-infection can determine the outcome of subsequent IAV infection by altering the airway microenvironment.

Human Herpesvirus-6 and Cytomegalovirus Dna Infection in Liver Donor Biopsies

Background: Herpesvirus reactivation is common after liver transplantation and co-infections with these viruses may manifest as febrile syndromes. A seropositive donor coupled with a seronegative recipient is a risk factor for primary CMV infection. Objective: Our study analyzed the presence of CMV and HHV-6 - DNA in liver donor biopsies. Methods: Seventy-one patients submitted to orthotopic liver transplant, were investigated for the presence of CMV and HHV-6 DNA and coinfection (both viruses' DNA in the same biopsy) in their liver donor biopsies, using the nested- PCR technique. The biopsies were collected from the organ before the transplant. The clinical donors' information was obtained by the State Health Transplant System, Sao Paulo, Brazil. Results: Forty-four (62%) donors were men and 27 (38 %) were women, almost all the donors were blood group O, with mean age from 18-50. Thirty-seven (52.1%) donors died due to traumatic brain injury. Nine (12.8%) biopsies were positive for CMV DNA and 32 (45%) were positive for HHV-6 DNA. The co-infection (CMV and HHV-6) was positive in 7/71 liver donor biopsies. Conclusions: Infection with CMV and HHV-6 as well as co-infection CMV/HHV-6 has been shown to be highly prevalent in liver donors studied representing a possible risk factor for opportunistic infections.

Acute Cytomegalovirus Infection Is Associated with Increased Frequencies of Activated and Apoptosis-Vulnerable T Cells in HIV-1-Infected Infants

Cytomegalovirus (CMV) coinfection is associated with infant HIV-1 disease progression and mortality. In a cohort of Kenyan HIV-infected infants, the frequencies of activated (CD38(+) HLA-DR(+)) and apoptosis-vulnerable (CD95(+) Bcl-2(-)) CD4(+) and CD8(+) T cells increased substantially during acute CMV infection. The frequency of activated CD4(+) T cells was strongly associated with both concurrent CMV coinfection (P = 0.001) and HIV-1 viral load (P = 0.05). The frequency of apoptosis-vulnerable cells was also associated with CMV coinfection in the CD4 (P = 0.02) and CD8 (P < 0.001) T cell subsets. Similar observations were made in HIV-exposed uninfected infants. CMV-induced increases in T cell activation and apoptosis may contribute to the rapid disease progression in coinfected infants.

CONGENITAL TRANSMISSION OF HUMAN IMMUNODEFICIENCY VIRUS, CYTOMEGALOVIRUS, AND TOXOPLASMOSIS IN A PREMATURE INFANT

We report a preterm infant with congenital HIV-1, CMV, and toxoplasmosis coinfection, whose mother succumbed to probable cerebral toxoplasmosis. Despite repeated neuroimaging, retinal examinations and infant serologic tests, during the first 36 days of life, there was no evidence of congenital toxoplasmosis. However, subsequent tests showed cerebral calcifications, bilateral chorioretinitis, antitoxoplasma IgM antibody, and Toxoplasma gondii DNA in the cerebrospinal fluid by polymerase chain reaction.

Cytomegalovirus, adenovirus, and polyomavirus co-infection among pediatric recipients of allogeneic stem cell transplantation: Characteristics and outcome

ADV and PMV infection have increasingly been documented as significant complications following allo-HSCT. Despite increasing recognition, characteristics and outcome of CMV, ADV, and PMV viral co-infection remain obscured. In this study, a retrospective quantitative PCR analysis of ADV, PMV (BKV and JCV) was performed from pediatric patients' stored blood samples previously tested for CMV viremia after allo-HSCT. Clinical and virological characteristics and outcome among patients with and without viral co-infection were analyzed and compared. From 2001 to 2006, 219 blood samples from 69 patients were studied. Viral DNA was present in 119 samples (52.9%).The proportion of viremia was highest for BKV (30.6%), followed by CMV (20.9%), ADV (9.1%), and JCV (0.5%). Viral co-infection occurred in 17 patients (24.6%), with CMV/BKV as the most common type (11.6%), followed by CMV/ADV (4.3%) and ADV/BKV (2.9%). From multivariate analysis, factors associated with viral co-infection were acute GVHD (OR 4.57; 95% CI 1.9-10.96, p = 0.001), level of blood CMV viral load (OR 1.53; 95% CI 1.24-1.89, p < 0.001), and level of blood ADV viral load (OR 1.56; 95% CI 1.05-2.32, p = 0.027). Higher probability of developing viral disease was strongly associated with more types of virus detected in blood (p < 0.001). Significant difference in the causes of death was observed among patients with and without viral co-infection (p = 0.014). Infection (87.5%) was the major cause of death of patients with viral co-infection, whereas relapse of hematologic disease (70%) was the major cause of death of patients with mono-viral infection. Viral co-infection is a common and significant infectious complication in pediatric recipients of allo-HSCT. Blood monitoring of CMV, ADV, and BKV is suggested among pediatric patients who develop GvHD or who have rising of CMV or ADV viremia following allo-HSCT.

Herpesvirus Seropositivity in Childhood Associates with Decreased Monocyte-Induced NK Cell IFN-γ Production

EBV infection is inversely associated with IgE sensitization in children, and this association is further enhanced by CMV coinfection. In mice, herpesvirus latency causes systemic innate activation and protection from bacterial coinfection, implying the importance of herpesviruses in skewing immune responses during latent infection. Early control of viral infections depends on IFN-gamma release by NK cells, which generally requires the presence of accessory cells. We investigated IFN-gamma production by NK cells in PBMCs from children seropositive (SP) for EBV alone, for both EBV and CMV, or seronegative for both viruses. The ability of classical (CD14(++)CD16(-)) and proinflammatory (CD14(+)CD16(+)) monocytes to induce autologous NK cell IFN-gamma was studied by coculture experiments with enriched CD3(-)CD56(+) cells. Transwell experiments were used to evaluate how monocytes interact with NK cells to induce IFN-gamma synthesis. SP children had a significantly reduced proportion of IFN-gamma(+) NK cells and cognate intracellular IFN-gamma levels, which was more pronounced in CMV-coinfected subjects. Also, resting PBMCs of SP children displayed lower proportions of proinflammatory monocytes. IFN-gamma production by NK cells was dependent on interactions with monocytes, with the proinflammatory subset inducing the highest IFN-gamma. Finally, SP children had markedly lower levels of plasma IFN-gamma, concurrent with in vitro findings. Herpesvirus infections could be one contributing factor for maturation toward balanced Th1-Th2 responses. Our data indicate that early infection by herpesviruses may affect NK cell and monocyte interactions and thereby also influence the development of allergies.

The impact of HIV infection on the nervous system of children

HIV affects the immature brain causing static or progressive encephalopathy (PE). PE is characterized by acquired microcephaly, failure to attain or loss of neurodevelopmental milestones, or loss of intellectual ability, and acquired symmetric motor defects. Isolated neurodevelopmental delays and peripheral nervous system disease occur as a direct consequence of HIV infection. Susceptibility to opportunistic infection (OI), due to systemic immunodeficiency, predisposes HIV-infected children to CNS infections including acute bacterial and tuberculous meningitis, CMV co-infection, EBV-associated primary lymphoma and in older children cryptococcal meningitis. HAART may induce an immune reconstitution inflammatory response to several microorganisms including mycobacterium tuberculosis and JC virus, causing CNS deterioration. Neurological manifestations occur in 20– 80% of HIV-infected children. Complex clinical presentations may be difficult to classify with the layering effect of multiple pathologies. There are limited descriptive studies from resource-constrained countries. In one hospitalbased, cross-sectional survey (n = 80, median age = 5.2 years), 60% had a variety of neurological and neurodevelopmental deficits. The neuropathogenesis of HIV encephalopathy is incompletely understood. Several pathogenic events are involved including (1) CNS invasion following receptor/ co-receptor-mediated HIV infection of monocytes/macrophages and CD4+ T-lymphocytes, (2) promotion of HIVinfected PBMC trafficking across the BBB by astrocytes and microglia (Trojan-horse effect), (3) neurotoxin elaboration induced by viral factors and inflammatory mediators, (4) CD4-independent astrocyte invasion by HIV, (4) neuronal death mediated through viral-induced chemokine receptor expression, and microglial/macrophagedependent and microglial-independent apoptotic death, and (5) inhibition of neural stem cell proliferation by viral gp120. Both direct and indirect mechanisms are involved in neuronal injury and death.

Acute respiratory failure due to Pneumocystis pneumonia: outcome and prognostic factors

To examine the outcome and prognostic factors of in-hospital mortality in patients with acute respiratory failure (ARF) caused by Pneumocystis pneumonia (PCP) admitted to a medical intensive care unit. A retrospective review was conducted of all patients with ARF from PCP in Ramathibodi Hospital between 2000 and 2006. Patient characteristics, clinical presentation, and laboratory, radiological and microbiological findings, as well as therapy and clinical course were included in the analysis of prognostic factors of death. A total of 14 HIV-infected and 30 otherwise immunosuppressed patients were identified. The overall mortality rate was 63.6%. Logistic regression analysis demonstrated that APACHE II score on day 1 and level of PEEP used on day 3 of respiratory failure were associated with higher hospital mortality. In a comparison between the HIV group and the non-HIV group, the early mortality rate was significantly higher in the HIV group, but late hospital mortality was not different between the two groups. Using a univariate logistic regression model, four parameters were found to be significantly associated with death in the HIV group: sex, APACHE II score on day 1, CMV co-infection, and level of PEEP on day 3 of ARF. In the non-HIV group, corticosteroid use prior to diagnosis of PCP and level of PEEP on day 3 of ARF were found to be the significant parameters. The mortality rate in patients with ARF caused by PCP was high. Various variable factors were related to a poor prognosis. For improved survival, multimodality treatments are needed to reduce these risk factors.