Differences in Expression of Selected Interleukins in HIV-Infected Subjects Undergoing Antiretroviral Therapy

The use of combined antiretroviral therapy (cART) inhibits the replication of the Human Immunodeficiency Virus (HIV) and thus may affect the functioning of the immune system, e.g., induce changes in the expression of certain cytokines. The aim was to examine the effect of cART on the expression of selected cytokines: interleukin -4, -7 and -15 in HIV-infected subjects. The test material was the plasma of HIV-infected men and healthy men (C, control group). The levels of interleukin were measured by immunoenzymatic method before cART and one year after treatment in relation to the C group. HIV-infected men were analyzed in subgroups depending on the HIV-RNA viral load, CD4⁺ and CD8⁺T-cell counts, and the type of therapeutic regimen. A significantly higher level of IL-4 was demonstrated in HIV-infected men before cART compared to those after treatment and in the control group. The use of cART resulted in a significant decrease in the level of IL-7 in HIV-infected men; however, high levels of IL-7 were associated with a low number of CD4⁺ T cells and CD8⁺ T cells. An increase in the level of IL-15 in HIV-infected men was noted after the use of cART. There was no difference in the expression of interleukins depending on the treatment regimen used. The study showed the effect of cART on the expression of interleukins, especially IL-4 and IL-7. Further research in this direction seems promising, confirming the role of these interleukins in the course of the disease.     

Varicella-zoster virus-specific cell-mediated immune responses in HIV-infected adults

The incidence of herpes zoster remains high in HIV-infected patients despite the use of combined antiretroviral therapy (cART). We wished to assess varicella-zoster virus (VZV)-specific cell-mediated immune (CMI) responses in HIV-infected adults on cART. VZV-specific CMI responses were assessed using lymphocyte proliferative responses, cytokine production (IL-2, TNF-α, and IFN-γ), and interferon-γ ELISPOT assays in 103 HIV-infected adults and 30 healthy controls. HIV-infected patients were analyzed according to their current and nadir CD4 cell count and their use of cART. A multivariate analysis was performed to identify factors associated with VZV-specific CMI responses. HIV-infected patients had lower VZV-specific CMI responses than healthy controls. Patients with a CD4 T cell count <100/μL had almost no detectable responses whereas those with a current CD4 T cell count >300/μL and suppressed viral replication on cART had responses similar to those of healthy controls. In multivariate analysis, factors significantly associated with VZV-specific CMI responses were the absence of a previous AIDS-defining event and higher CD4 cell counts, in particular central and effector memory CD4 T cell counts. HIV-infected patients with a history of AIDS or low CD4 cell counts have impaired VZV-specific CMI responses, and remain at risk for herpes zoster.     

No Differences of Immune Activation and Microbial Translocation Among HIV-infected Children Receiving Combined Antiretroviral Therapy or Protease Inhibitor Monotherapy

This is a cross-sectional study of 15 aviremic chronic HIV-infected children revealing no differences in immune activation (IA; HLA-DR⁺CD38⁺ CD4⁺ and CD8⁺ T cells, and sCD14) and microbial translocation (MT; lipopolysaccharides (LPS) and 16S rDNA) among HIV-infected patients under combined antiretroviral treatment (cART; n = 10) or ritonavir-boosted protease inhibitor monotherapy (mtPI/rtv; n = 5). In both cases, IA and MT were lower in healthy control children (n = 32). This observational study suggests that ritonavir boosted protease inhibitor monotherapy (mtPI/rtv) is not associated with an increased state of IA or MT as compared with children receiving cART.     

Oral environment and taste function of Japanese HIV-infected patients treated with antiretroviral therapy

ABSTRACT

The aim of the study was to evaluate the oral environment and the taste function of Japanese HIV-infected patients treated with antiretroviral therapy. Their median age of 73 patients taking anti-HIV drugs was 46 years. The median period of taking anti-HIV drugs was 30 months. The oral condition was evaluated by measurement of oral moisture, amount of saliva secretion, the number of oral bacteria, presence of oral candida, a taste test, and the number of missing teeth. The levels of oral moisture and secreted saliva were significantly lower in the HIV-infected group than in the healthy volunteer (control) group. The HIV-infected group showed a more robust decrease in taste sensation than the control group. The number of missing teeth was significantly higher in the HIV-infected group than in the control group. Furthermore, all of the evaluated oral conditions were worse in the HIV-infected patients whose CD4+ T lymphocyte counts were less than 500/mm³ than in the control group. It became clear that the patients taking anti-HIV drugs, especially the CD4+ count?<?500/mm3 group, had a deteriorated oral environment and dysgeusia, suggesting that the management of oral hygiene is necessary to maintain oral health, which leads to systemic health.     

When to Start Antiretroviral Therapy

Antiretrovirals perform superbly in combating HIV infection. But when to initiate therapy in asymptomatic, nonpregnant, hepatitis-free, HIV-infected persons is not securely established. Of two completed randomized trials using modern therapy, a Haitian trial demonstrated a benefit to initiating therapy between 200 and 350 CD4 cells/mm³ as compared with less than 200 CD4 cells/mm³ and an international trial demonstrated a benefit to starting at greater than 350 CD4 cells/mm³ as compared with less than 250 CD4 cells/mm³. Many observational cohorts support initiating treatment at less than 350 CD4 cells/mm³. Of these, three large studies supported initiation at less than 350 cells/mm³, less than 450 CD4 cells/mm³, and less than 500 CD4 cells/mm³, respectively, but only the last supported starting at higher counts. Such studies are not probative, given the problem of confounding. No conventional antiretroviral regimen is free of long-term adverse effects, especially over decades of use. All are expensive and require expensive monitoring. When resources are restricted, initiation of antiretrovirals for persons with high CD4 count diverts treatment from more needy persons. Pathophysiological considerations favor universal treatment because antiretrovirals mitigate systemic inflammation, which aggravates atherosclerosis. There are suggestions that HIV hastens the natural decline of cognitive, renal, and pulmonary function as well as bone mineral loss; the mechanism(s) are uncertain, as is the ability of antiretrovirals to counteract the probable acceleration. The four major guideline panels, although all have issued updates in the past year, are not consistent in recommendations for treatment of HIV-infected persons with counts greater than 350 CD4 cells/mm³.     

The long-term outcome of HIV-infected patients after intensive care admission

Long-term outcomes of HIV-infected patients admitted to the intensive care unit (ICU) since the advent of combination antiretroviral therapy (cART) have not been well described. We reviewed the long-term outcomes and clinical follow-up of HIV-infected patients admitted to the Prince of Wales Hospital ICU between 1999 and 2005 by a retrospective medical record review. Mortality was assessed in the ICU, in hospital and in the long-term. Twenty-four HIV-infected male patients underwent 26 ICU admissions. Their ICU and in-hospital mortalities were 33% and 46%, respectively. Higher APACHE (acute physiology and chronic health evaluation) II scores (median 27 versus 12, P < 0.001), lower CD4 cell counts (median 45 versus 335 cells/μL, P = 0.041) and longer hospitalization times prior to ICU admission (median 4 versus 1 day, P = 0.02) were significantly associated with in-hospital mortality. We found 85% of the subjects who survived hospital admission were still alive at a median of 41 months (4 months to 5 years) of follow-up, all of who were functionally independent. HIV-infected patients who survived ICU admission at our institution had good long-term outcomes in the cART era.     

Australian prescribers' perspectives on ART initiation in the era of “treatment as prevention”

This study explores Australian prescribers' attitudes towards Treatment as Prevention (TasP) and their practices around initiating combination antiretroviral treatment (cART) for HIV. A brief online survey was conducted nationally amongst antiretroviral treatment (ART) prescribers in Australia. The sample broadly represented ART prescribers in Australia (N = 108), with 40.7% general practitioners (GPs), 25.9% sexual health clinic-based physicians and 21.3% hospital-based infectious diseases physicians. About 60% of respondents had been treating HIV-positive patients for more than 10 years. Respondents estimated that about 70–80% of all their HIV-positive patients were receiving ART. Over half of the prescribers agreed very strongly that their primary concern in recommending cART initiation was clinical benefit to individual patients rather than any population benefit. A majority of the prescribers (68.5%) strongly endorsed cART initiation before CD4+ T-cell count drops below 350 cells/mm³, and a further 22.2% strongly endorsed cART initiation before CD4+ T-cell count drops below 500 cells/mm³. Regarding the optimal timing of cART initiation, this study shows that prescribers in Australia in 2012 focus primarily on the benefits for their individual patients. Prescribers may need more convincing evidence of individual health benefits or increased knowledge about the population health benefits for a TasP approach to be effective in Australia.     

Long-term trends in CD4 cell counts and impact of viral failure in individuals starting antiretroviral therapy: UK Collaborative HIV Cohort (CHIC) study

Objective

The aim of the study was to describe trends in CD4 cell counts in HIV‐infected patients after initiation of combination antiretroviral therapy (cART), according to CD4 cell count at initiation (baseline), and to quantify the implications of virological failure for these trends.

Methods

Eligible participants from the UK Collaborative HIV Cohort (CHIC) were antiretroviral‐naïve and started cART after 1997. Random effects were used to model CD4 cell count trends, accounting for multiple measurements within participants. We assessed whether CD4 cell count trends varied according to baseline CD4 cell count and separately in participants with and without post‐cART virological failure. Effects of post‐cART virological failure (>1000 HIV‐1 RNA copies/mL) on subsequent CD4 cell counts were evaluated.

Findings

A total of 7069 participants were included in the analysis (median follow‐up in all baseline CD4 cell count groups was ≥35 months). Among participants without virological failure ≥6 months after the start of cART, CD4 cell counts continued to increase up to 8 years, with little evidence that differences between baseline CD4 cell count groups diminished over time. Virological failure ≥6 months after the start of cART was associated with lower subsequent CD4 cell counts, with greater CD4 cell count reduction for more recent virological failure and higher viral load.

Conclusions

Post‐cART CD4 cell counts are strongly related to pre‐cART CD4 cell counts. CD4 cell count recovery is greatest in individuals who can avoid viral loads >1000 copies/mL while on cART.     

Highly Active Antiretroviral Therapy (HAART)-Related Hypertriglyceridemia Is Associated With Failure of Recovery of CD14lowCD16+ Monocyte Subsets in AIDS Patients

As cellular reservoirs, CD16⁺ monocyte subsets play important roles in the progression of HIV infection. Previous studies have shown that highly active antiretroviral therapy (HAART) reduced the percentages of CD14^highCD16⁺ monocyte subsets, but did not recover the percentages of CD14^lowCD16⁺ subsets. Eighty-four chronic HIV-infected, HAART-naïve individuals and 55 HIV-negative subjects (31 without hyperlipidemia and 24 with hypertriglyceridemia) were enrolled. Plasma HIV-1 RNA levels, CD4⁺ T-cell counts, triglycerides, total cholesterol, high-density lipoprotein, and low-density lipoprotein were followed up for 48 weeks during HAART treatment in the longitudinal study. We found that mild hypertriglyceridemia in HIV-negative subjects and HIV-infected patients, naïve to HAART, did not affect the percentage of monocyte subsets. However, a failure of CD14^lowCD16⁺ subset recovery was observed in patients with HAART-related hypertriglyceridemia at 48 weeks. Thus, HAART-related hypertriglyceridemia altered homeostasis of monocyte subsets to antiviral therapy, which might further affect immune reconstitution.     

From the Cover: Clonally expanded CD4+ T cells can produce infectious HIV-1 in vivo

Reservoirs of infectious HIV-1 persist despite years of combination antiretroviral therapy and make curing HIV-1 infections a major challenge. Most of the proviral DNA resides in CD4⁺T cells. Some of these CD4⁺T cells are clonally expanded; most of the proviruses are defective. It is not known if any of the clonally expanded cells carry replication-competent proviruses. We report that a highly expanded CD4⁺ T-cell clone contains an intact provirus. The highly expanded clone produced infectious virus that was detected as persistent plasma viremia during cART in an HIV-1–infected patient who had squamous cell cancer. Cells containing the intact provirus were widely distributed and significantly enriched in cancer metastases. These results show that clonally expanded CD4⁺T cells can be a reservoir of infectious HIV-1.HIV-1 infection can be controlled, but not cured, by combination antiretroviral therapy (1); cells infected with replication-competent HIV-1 persist despite many years of combination antiretroviral therapy (cART). Recently, we and others (2, 3) showed that there is frequent clonal expansion of HIV-1–infected cells in patients and that these clones can persist for more than 10 y. Most of the proviruses that persist in patients on cART are defective (4), and it is not known whether clonally expanded cells can harbor a replication-competent provirus. It has been suggested that CD4⁺ T-cell clones are not likely to contain replication-competent HIV-1 because expression of viral proteins is cytotoxic, and the host’s immune system would preferentially eliminate infected cells that express viral proteins (4). Only a small proportion of integrated proviruses are intact (4), and it has been proposed that clonally expanded CD4⁺ T cells contain only defective proviruses and that intact proviruses that make up the reservoir are found only in unexpanded cells (5). Previous studies have reported that populations of virus with identical sequences emerge in the plasma after several years of suppressive cART (6, 7), but it is not known whether the identical viruses found in the blood of patients are infectious. We report here the identification of a highly expanded clone of HIV-infected CD4⁺ T cells that produced infectious virus at a level that caused persistent plasma viremia. This result shows that cells containing replication-competent HIV-1 proviruses can clonally expand and persist in vivo, presenting a challenge for achieving a cure of HIV-1 infection.     

Coinfection by HTLV-I/II is associated with an increased risk of strongyloidiasis and delay in starting antiretroviral therapy for AIDS patients

ObjectiveTo compare the clinical characteristics and outcomes of HIV-1-HTLV-1 coinfected patients, in Bahia, Brazil.MethodsRetrospective, comparative study.ResultsAmong a total of 123 consecutive HIV infected patients, 20 men (20.6%) and 6 women (23.1%) had detectable antibodies against HTLV-I/II. The major risk factor associated with coinfection by HTLV was intravenous drug use (57.7% of coinfected patient versus 9.2% of HTLV seronegative patients, p < 0.0001). Coinfected patients had higher absolute lymphocyte counts (1,921 + 762 versus 1,587 + 951, p = 0.03). Both groups of patients had similar means of CD4+ and CD8+ cell counts. However, among patients with AIDS CD4+ cell counts were significantly higher among those coinfected with HTLV-I/II (292 ± 92 cells/mm³, versus 140 ± 177cells/mm³, p = 0.36). The frequency and type of opportunistic infections were similar for both groups, but strongyloidiasis and encephalopathy were more frequently diagnosed in coinfected patients (p < 0.05). On the other hand, patients coinfected with HTLV-I/II received significantly less antiretroviral therapy than singly infected by HIV-1ConclusionCoinfection by HTLV-I/II is associated with an increased risk of strongyloidiasis for HIV patients. Higher CD4 count may lead to underestimation of immunodeficiency, and delay to initiate antiretroviral therapy.     

Executive summary. Consensus document of GESIDA and SPNS (Spanish Secretariat for the National Plan on AIDS) regarding combined antiretroviral treatment in adults infected by the human immunodeficiency virus (January 2012)

In the present update of the guidelines, starting antiretroviral treatment is recommended in symptomatic patients, in pregnant women, in sero-discordant couples with high transmission risk, in patients co-infected with hepatitis B requiring treatment and in patients with HIV-related nephropathy. Guidelines on combined antiretroviral treatment (cART) are included in the event of concurrent HIV infection diagnosis with an AIDS-defining event. In asymptomatic naïve patients, cART will be based on CD4 lymphocyte count, plasma viral load (VL), patient age and patient comorbidity: (i) cART is recommended if CD4 count is lower than 350 cells/μL; (ii) cART is equally recommended if CD4 count is between 350 and 500 cells/μL and may only be deferred in the event of patient refusal with stable CD4 count and low VL; (iii) if CD4 count is higher than 500 cells/μL cART can be delayed, but it may be considered in patients with liver cirrhosis, chronic virus C hepatitis, high cardiovascular risk, VL >10⁵ copies/mL, CD4 proportion lower than 14% and age over 55 years. cART in naïve patients requires a combination of three drugs and its aim is to achieve undetectable VL. Treatment adherence plays a basic role in sustaining good response. cART could and should be changed if virologic failure occurs in order to achieve undetectable VL again. Approaches to cART in HIV acute infection, in women and pregnancy and post exposure prophylaxis are also commented on.     

Diagnosing HIV-Related disease

OBJECTIVE: To summarize current information on the relation between CD4 counts and the risk of different HIV-related diseases. MEASUREMENTS AND MAIN RESULTS: MEDLINE search of English language articles between 1985 and 1996 using the medical subject heading (MeSH) term “CD4 lymphocyte count” and searches using key words of multiple HIV-related diseases were conducted. Some HIV-related diseases can be stratified to different CD4 count levels. Regardless of their CD4 count, HIV-infected patients are susceptible to sinusitis, Kaposi’s sarcoma, community-acquired pneumonia, and oral hairy leukoplakia. In advanced HIV, when CD4 is below 200/mm³, Pneumocystis carinii pneumonia, toxoplasmosis, progressive multifocal leukoencephalopathy, Mycobacterium avium complex, molluscum contagiosum, and bacillary angiomatosis all increase in incidence. In very advanced HIV disease, when CD4 counts are below 50/mm³, patients are at risk of pseudomonas pneumonia, cytomegalovirus retinitis, central nervous system lymphoma, aspergillosis, and disseminated histoplasmosis. Summary  Regardless of their CD4 count, HIV-infected patients are susceptible to sinusitis, community-acquired pneumonia, oral hairy leukoplakia, Kaposi’s sarcoma, and HIV meningitis. Once their CD4 counts drop below 500/mm³, they are at risk of developing tuberculosis, thrush, herpes simplex, and herpes zoster. In advanced HIV, when their CD4 counts are below 200/mm³, PCP, coccidioidomycosis, bacillary angiomatosis, molluscum contagiosum, cryptococcal meningitis, toxoplasmosis, progressive multifocal leukoencephalopathy, Mycobacterium avium complex, and non-Hodgkin’s lymphoma all increase in incidence. In very advanced HIV, when their CD4 counts are below 50/mm³, they are at risk of pseudomonas pneumonia, CMV retinitis, CNS lymphoma, aspergillosis, and histoplasmosis. By appreciating these characteristic changes in disease incidence, and by knowing a patient’s CD4 count, clinicians should be better able to develop differential diagnoses and plans for diagnostic evaluation. Received from the Department of Medicine, University of Washington, Seattle.     

Inconsistent reconstitution of cytomegalovirus-specific cell-mediated immunity in human immunodeficiency virus-infected patients receiving highly active antiretroviral therapy

Cytomegalovirus (CMV)-immune recovery was characterized in human immunodeficiency virus (HIV)-infected patients receiving highly active antiretroviral therapy. CMV lymphocyte proliferation (LP), responder-cell frequency (RCF), and interferon (IFN)-gamma and interleukin (IL)-2 secretion were studied in CMV-seropositive HIV-infected patients and in CMV-seropositive HIV-uninfected control subjects. HIV-infected patients and control subjects had similar proportions of IL-2 and IFN-gamma, but levels were lower in HIV-infected patients. LP and RCF were significantly less frequent and of lower magnitude in HIV-infected patients. The measures of CMV cell-mediated immunity were correlated in HIV-uninfected but not in HIV-infected subjects. To investigate this, IL-2, IL-12, anti-CD28 plus anti-CD49d, or anti-IL-10 was added in vitro, with no effect on LP. However, CD8 cell depletion of mononuclear cells from HIV-infected patients increased LP responses to levels similar to those of uninfected control subjects; before depletion, only RCF correlated with CD4 cell counts, but after depletion, LP also correlated with CD4 cell counts.     

Serum leptin and CD4+ T lymphocytes in HIV+ children during highly active antiretroviral therapy

objective Because leptin, the adipocyte‐derived hormone, affects thymocyte survival, proliferation of naïve T lymphocytes and the production of proinflammatory cytokines, we aimed to investigate the role of this molecule in immunoreconstitution during highly active antiretroviral therapy (HAART). design Prospective longitudinal cohort study. A series of 20 HIV⁺ children were studied. The subjects were grouped by their increase in serum leptin levels after HAART. methods All participants were weight‐stable, free of endocrine disorders and opportunistic infections and equally distributed for sex (males, n= 10; females, n= 10). Body mass index (BMI), serum lipids, leptin, CD4⁺ T cells and HIV‐1 RNA were measured before initiation of HAART and after a 2‐year follow‐up. results Serum leptin concentration positively correlated with CD4⁺ lymphocyte number before treatment. HAART significantly reduced viraemia and increased serum levels of lipids in all patients, whereas a significant increase in CD4⁺ cells and serum leptin was observed in the majority of patients. Notably, in children where HAART was not effective in increasing CD4⁺ lymphocyte counts, serum leptin did not increase. conclusion To our knowledge, these findings reveal for the first time a novel link among CD4⁺ T lymphocytes, serum leptin and highly active anteretroviral theraphy.     

Granulomatous Pneumocystis jiroveci pneumonia associated with immune reconstituted HIV

Pneumocystis jiroveci pneumonia uncommonly presents with pulmonary nodules and granulomatous inflammation. An unusual case of granulomatous P jiroveci pneumonia in an HIV patient with a CD4⁺ lymphocyte count of greater than 200 cells/mm³, occurring in the context of immune reconstitution with highly active antiretroviral therapy, is described. The case highlights the importance of establishing this diagnosis to institute appropriate therapy.     

Clinical outcome of HIV-infected haemophiliac patients in Hong Kong

Summary . About half of the haemophiliacs in Hong Kong have been infected by human immunodeficiency virus (HIV). This study aimed to determine their clinical course of progression. Forty-seven adult patients with congenital coagulation factor deficiency being followed up regularly from January 1992 onward in the Department of Medicine of Queen Mary Hospital, Hong Kong, were included in this study. Twenty were positive for HIV antibody and the remaining 27 were negative. Three other HIV-positive patients who died before 1992 were excluded. From January 1992 to June 1996, the 47 patients included in the study were followed up in the clinic every 3–6 months with regular CD4, CD8 lymphocyte counts and β2 microglobulin levels. At the initiation of the study in January 1992, the HIV-infected patients had already a lower mean CD4 count (360.4 μL^?1 versus 658.8 μL^?1, P<0.01), a reversed CD4/CD8 ratio (0.53) and a higher mean serum β2 microglobulin level (1.853 μg mL^?1 versus 1.315 μg mL^?1, P>0.05). On regular follow-up, HIV-positive patients had a more significant progressive fall in their mean CD4 count (301.6 μL^?1 versus 360.4 μL^?1, P<0.01) and rise in their mean serum β2 microglobulin level (2.60 μg mL^?1, versus 1.853 μg mL^?1, P<0.05). The CD4 and CD8 counts of HIV-positive patients were falling at a rate of 1.44 μL^?1 month^?1 and 4.03 μL^?1 month^?1 respectively. During the follow-up period, two of the 20 HIV-positive patients developed clinical acquired immunodeficiency syndrome (AIDS) at 15 and 36 months from the initiation of the study. Both patients had typical features of AIDS with a low CD4 count, reversed CD4/CD8 ratio and elevated β2 microglobulin level. The former patient eventually died of fungal brain abscess. The remaining 18 HIV-positive patients so far remained clinically asymptomatic. Eleven patients were put on antiretroviral drug therapy when their CD4 counts fell below 200 μL^?1. Only two of the 20 HIV-infected patients developed AIDS during the observation period of 4 years; this figure of 10% is relatively slow. Two of our patients died of AIDS before the study was initiated in 1992. Even if they were included, still only 17.4% had progressed. The figure is in the lowest rate of progression expected from Western experience. Although our study population is small, it remains unclear why our HIV-infected Chinese haemophiliacs have a slow rate of progression to AIDS.     

Lymphopenic community-acquired pneumonia is associated with a dysregulated immune response and increased severity and mortality

ObjectivesLymphopenic (<724 lymphocytes/µL) community-acquired pneumonia (L-CAP) is an immunophenotype with an increased risk of mortality. We aimed to characterize the l-CAP immunophenotype though lymphocyte subsets and the inflammatory response and its relationship with severity at presentation and outcome.MethodsProspective study of 217 immunocompetent patients hospitalized for CAP. Lymphocyte subsets (CD4⁺, CD8⁺, CD19⁺, and natural killer [NK] cells) and inflammatory cytokines were analyzed on days 1 and 4, and immunoglobulin subclasses were analyzed on day 1 in a nested group.Results39% of patients showed l-CAP, with decreased levels of all lymphocyte subsets with a partial recovery of CD4⁺ and CD8⁺ cells by day 4. l-CAP patients exhibited higher initial severity and systemic levels of interleukin (IL)-8, IL-10, granulocyte colony-stimulating factor, and monocyte chemoattractant protein-1. Initial IgG2 levels were lower in patients with <724 lymphocytes/µL and positively correlated with ALC, CD4⁺, and CD19⁺ cell counts. Low CD4⁺ counts (<129 cells/µL) also independently predicted 30-day mortality after adjusting for age, gender, and the CURB-65 score.Conclusionsl-CAP is characterized by CD4⁺ depletion, a higher inflammatory response, and low IgG2 levels that correlated with greater severity at presentation and worse prognosis. l-CAP is an immunophenotype useful for rapidly recognizing severity.     

Réactivation d’une infection à parvovirus B19 chez une patiente infectée par le VIH

Introduction

Infection by human parvovirus B19 (erythrovirus B19) is common and usually asymptomatic during childhood conferring lasting protection against a new infection. Parvovirus B19 infection may cause erythema infectiosum (5th disease) and aplastic crisis. Secondary symptomatic parvovirus B19 infection in the same patient is rare and its physiopathology is not always clear.

Case report

A 48-year-old HIV-infected female patient presented within 5 years two acute episodes of parvovirus B19 infection although her CD4 cells count was above 500/mm³. Absence of specific antibodies production after the first episode and persisting parvovirus viremia suggested viral reactivation rather than re-infection. During the second episode, specific antibodies were produced.

Conclusion

Similarly to most DNA viruses, parvovirus B19 reactivation is possible in HIV-infected patients while effectively treated by antiretroviral therapy.