scholarly journals Acute Human Immunodeficiency Virus (HIV) Infection Presenting With Bilateral Interstitial Pneumonia: Case Report and Discussion of Potential HIV-Induced Interstitial Pneumonia

2017 ◽  
Vol 4 (4) ◽  
Author(s):  
Anna Maria Peri ◽  
Laura Alagna ◽  
Serena Trovati ◽  
Francesca Sabbatini ◽  
Roberto Rona ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Human Immunodeficiency Virus ◽  
Intensive Care ◽  
Case Report ◽  
Interstitial Pneumonia ◽  
Antiretroviral Treatment ◽  
Pneumonia Case ◽  
Immunodeficiency Virus ◽  
Acute Hiv ◽  
Hiv 1

Abstract A 50-year-old man was admitted to intensive care unit because of acute respiratory failure due interstitial pneumonia; after admission, a diagnosis of acute human immunodeficiency virus (HIV)-1 infection was made. Clinical and radiological improvement was observed only after introduction of antiretroviral treatment. We discuss the hypothesis of interstitial pneumonia induced by the acute HIV-1 infection.

scholarly journals Novel Inhibitory Effects of γ-Glutamylcysteine Ethyl Ester against Human Immunodeficiency Virus Type 1 Production and Propagation

1998 ◽  
Vol 42 (5) ◽  
pp. 1200-1206 ◽  
Author(s):  
Satoshi Kubota ◽  
Shubhra Shetty ◽  
Huizhong Zhang ◽  
Shigehisa Kitahara ◽  
Roger J. Pomerantz
Keyword(s):  
Human Immunodeficiency Virus ◽  
Ethyl Ester ◽  
Human Immunodeficiency Virus Type ◽  
Inhibitory Effects ◽  
Immunodeficiency Virus ◽  
Acute Hiv ◽  
High Doses ◽  
Anti Hiv ◽  
Hiv 1

ABSTRACT The anti-human immunodeficiency virus type I (anti-HIV-1) effects of γ-glutamylcysteine ethyl ester (γ-GCE; TEI-2306) were examined in vitro. In initial studies using a vigorously HIV-1-producing human T-lymphocytic cell line, γ-GCE displayed a novel biphasic repressive effect on chronic HIV-1 infection that was unlike that of other glutathione prodrugs or other reported antioxidants. In high doses, up to a concentration of 2.5 mM, at which neither glutathione (GSH) nor another GSH precursor has shown inhibitory effects, γ-GCE potently inhibited the production of HIV-1 by a selective cytopathic effect against infected cells, while the viability and growth of uninfected cells were unaffected at the same γ-GCE concentrations. At lower concentrations (200 to 400 μM), γ-GCE significantly repressed the virus production from chronically HIV-1-expressing cells without affecting their viability. The discrepancy of the thresholds of the toxic doses between infected and uninfected cells was found to be more than 10-fold. Relatively high doses of γ-GCE, utilized in acute HIV-1 infection of T-lymphocytic cells, entirely blocked the propagation of HIV-1 and rescued the cells from HIV-1-induced cell death. Furthermore, γ-GCE at such concentrations was found to directly inhibit the infectivity of HIV-1 within 4 h. Repressive effects of γ-GCE on acute HIV-1 infection in human primary human peripheral blood mononuclear cells were also demonstrated. Here, the anti-HIV-1 strategy utilizing γ-GCE is removal of both HIV-1-producing cells and free infectious HIV-1 in vitro, in place of specific immunoclearance in vivo, which might lead to an arrest or slowing of viral propagation in HIV-1-infected individuals.

scholarly journals Activities of the human immunodeficiency virus type 1 (HIV-1) protease inhibitor nelfinavir mesylate in combination with reverse transcriptase and protease inhibitors against acute HIV-1 infection in vitro.

1997 ◽  
Vol 41 (10) ◽  
pp. 2159-2164 ◽  
Author(s):  
A K Patick ◽  
T J Boritzki ◽  
L A Bloom
Keyword(s):  
Human Immunodeficiency Virus ◽  
Protease Inhibitors ◽  
Drug Combination ◽  
Cellular Cytotoxicity ◽  
Immunodeficiency Virus ◽  
Nelfinavir Mesylate ◽  
Acute Hiv ◽  
Hiv 1

Nelfinavir mesylate (formerly AG1343) is a potent and selective, nonpeptidic inhibitor of human immunodeficiency virus type 1 (HIV-1) protease that was discovered by protein structure-based design methodologies. We evaluated the antiviral and cytotoxic effects of two-drug combinations of nelfinavir with the clinically approved antiretroviral therapeutics zidovudine (ZDV), lamivudine (3TC), dideoxycytidine (ddC; zalcitabine), stavudine (d4T), didanosine (ddI), indinavir, saquinavir, and ritonavir and a three-drug combination of nelfinavir with ZDV and 3TC against an acute HIV-1 strain RF infection of CEM-SS cells in vitro. Quantitative assessment of drug interaction was evaluated by a universal response surface approach (W. R. Greco, G. Bravo, and J. C. Parsons, Pharm. Rev. 47:331-385, 1995) and by the method of M. N. Prichard and C. Shipman (Antiviral Res. 14:181-206, 1990). Both analytical methods yielded similar results and showed that the two-drug combinations of nelfinavir with the reverse transcriptase inhibitors ZDV, 3TC, ddI, d4T, and ddC and the three-drug combination with ZDV and 3TC resulted in additive to statistically significant synergistic interactions. In a similar manner, the combination of nelfinavir with the three protease inhibitors resulted in additive (ritonavir and saquinavir) to slightly antagonistic (indinavir) interactions. In all combinations, minimal cellular cytotoxicity was observed with any drug alone and in combination. These results suggest that administration of combinations of the appropriate doses of nelfinavir with other currently approved antiretroviral therapeutic agents in vivo may result in enhanced antiviral activity with no associated increase in cellular cytotoxicity.

scholarly journals Induction of a Striking Systemic Cytokine Cascade prior to Peak Viremia in Acute Human Immunodeficiency Virus Type 1 Infection, in Contrast to More Modest and Delayed Responses in Acute Hepatitis B and C Virus Infections

2009 ◽  
Vol 83 (8) ◽  
pp. 3719-3733 ◽  
Author(s):  
Andrea R. Stacey ◽  
Philip J. Norris ◽  
Li Qin ◽  
Elizabeth A. Haygreen ◽  
Elizabeth Taylor ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hepatitis B ◽  
Human Immunodeficiency Virus Type ◽  
Plasma Viremia ◽  
Cytokines And Chemokines ◽  
Immunodeficiency Virus ◽  
Acute Hiv ◽  
Cytokine Cascade ◽  
Hiv 1

ABSTRACT Characterization of the immune responses induced in the initial stages of human immunodeficiency virus type 1 (HIV-1) infection is of critical importance for an understanding of early viral pathogenesis and prophylactic vaccine design. Here, we used sequential plasma samples collected during the eclipse and exponential viral expansion phases from subjects acquiring HIV-1 (or, for comparison, hepatitis B virus [HBV]or hepatitis C virus [HCV]) to determine the nature and kinetics of the earliest systemic elevations in cytokine and chemokine levels in each infection. Plasma viremia was quantitated over time, and levels of 30 cytokines and chemokines were measured using Luminex-based multiplex assays and enzyme-linked immunosorbent assays. The increase in plasma viremia in acute HIV-1 infection was found to be associated with elevations in plasma levels of multiple cytokines and chemokines, including rapid and transient elevations in alpha interferon (IFN-α) and interleukin-15 (IL-15) levels; a large increase in inducible protein 10 (IP-10) levels; rapid and more-sustained increases in tumor necrosis factor alpha and monocyte chemotactic protein 1 levels; more slowly initiated elevations in levels of additional proinflammatory factors including IL-6, IL-8, IL-18, and IFN-γ; and a late-peaking increase in levels of the immunoregulatory cytokine IL-10. Notably, there was comparatively little perturbation in plasma cytokine levels during the same phase of HBV infection and a delayed response of more intermediate magnitude in acute HCV infection, indicating that the rapid activation of a striking systemic cytokine cascade is not a prerequisite for viral clearance (which occurs in a majority of HBV-infected individuals). The intense early cytokine storm in acute HIV-1 infection may have immunopathological consequences, promoting immune activation, viral replication, and CD4+ T-cell loss.

Pharmacological Considerations in Human Immunodeficiency Virus–Infected Adults in the Intensive Care Unit

2013 ◽  
Vol 33 (2) ◽  
pp. 46-56 ◽  
Author(s):  
Ashley A. DeFreitas ◽  
Theresa-Lynda M. D’Souza ◽  
Ginille J. Lazaro ◽  
Emily M. Windes ◽  
Melissa D. Johnson ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Human Immunodeficiency Virus ◽  
Intensive Care ◽  
Immunodeficiency Virus

scholarly journals Human Immunodeficiency Virus Type 1 Monoclonal Antibodies Suppress Acute Simian-Human Immunodeficiency Virus Viremia and Limit Seeding of Cell-Associated Viral Reservoirs

2015 ◽  
Vol 90 (3) ◽  
pp. 1321-1332 ◽  
Author(s):  
Diane L. Bolton ◽  
Amarendra Pegu ◽  
Keyun Wang ◽  
Kathleen McGinnis ◽  
Martha Nason ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Clinical Trials ◽  
Monoclonal Antibodies ◽  
Antiretroviral Therapy ◽  
Envelope Glycoprotein ◽  
Plasma Viremia ◽  
Immunodeficiency Virus ◽  
Acute Hiv ◽  
Hiv 1

ABSTRACTCombination antiretroviral therapy (cART) administered shortly after human immunodeficiency virus type 1 (HIV-1) infection can suppress viremia and limit seeding of the viral reservoir, but lifelong treatment is required for the majority of patients. Highly potent broadly neutralizing HIV-1 monoclonal antibodies (MAbs) can reduce plasma viremia when administered during chronic HIV-1 infection, but the therapeutic potential of these antibodies during acute infection is unknown. We tested the ability of HIV-1 envelope glycoprotein-specific broadly neutralizing MAbs to suppress acute simian-human immunodeficiency virus (SHIV) replication in rhesus macaques. Four groups of macaques were infected with SHIV-SF162P3 and received (i) the CD4-binding-site MAb VRC01; (ii) a combination of a more potent clonal relative of VRC01 (VRC07-523) and a V3 glycan-dependent MAb (PGT121); (iii) daily cART, all on day 10, just prior to expected peak plasma viremia; or (iv) no treatment. Daily cART was initiated 11 days after MAb administration and was continued for 13 weeks in all treated animals. Over a period of 11 days after a single administration, MAb treatment significantly reduced peak viremia, accelerated the decay slope, and reduced total viral replication compared to untreated controls. Proviral DNA in lymph node CD4 T cells was also diminished after treatment with the dual MAb. These data demonstrate the virological effect of potent MAbs and support future clinical trials that investigate HIV-1-neutralizing MAbs as adjunctive therapy with cART during acute HIV-1 infection.IMPORTANCETreatment of chronic HIV-1 infection with potent broadly neutralizing HIV-1 MAbs has been shown to significantly reduce plasma viremia. However, the antiviral effect of MAb treatment during acute HIV-1 infection is unknown. Here, we demonstrate that MAbs targeting the HIV-1 envelope glycoprotein both suppress acute SHIV plasma viremia and limit CD4 T cell-associated viral DNA. These findings provide support for clinical trials of MAbs as adjunctive therapy with antiretroviral therapy during acute HIV-1 infection.

scholarly journals HIV treatment non-adherence is associated with ICU mortality in HIV-positive critically ill patients

2020 ◽  
pp. 175114371989897 ◽  
Author(s):  
Nelson BF Neto ◽  
Luiz G Marin ◽  
Bruna G de Souza ◽  
Ana LD Moro ◽  
Wagner L Nedel
Keyword(s):  
Intensive Care Unit ◽  
Human Immunodeficiency Virus ◽  
Intensive Care ◽  
Antiretroviral Therapy ◽  
Intensive Care Unit Admission ◽  
Hospital Mortality ◽  
Intensive Care Units ◽  
Therapy Adherence ◽  
Antiretroviral Therapy Adherence ◽  
Immunodeficiency Virus

Introduction Combined antiretroviral therapy has led to significant decreases in morbidity and mortality in acquired immunodeficiency syndrome patients. Survival among these patients admitted to intensive care units has also improved in the last years. However, the prognostic predictors of human immunodeficiency vírus patients in intensive care units have not been adequately studied. The main objective of this study was to evaluate if non-adherence to antiretroviral therapy is a predictor of hospital mortality. Methods A unicentric, retrospective, cohort study composed of patients admitted to a 59-bed mixed intensive care unit including all patients with human immunodeficiency vírus infection. Patients were excluded if exclusive palliative care was established before completing 48 h of intensive care unit admission. Clinical and treatment data were obtained, including demographic records, underlying diseases, Simplified Acute Physiology III score at the time of intensive care unit admission, CD4 lymphocyte count, antiretroviral therapy adherence, admission diagnosis, human immunodeficiency vírus-related diseases, sepsis and use of mechanical ventilation and hemodialysis. The outcome analyzed was hospital mortality. Results Overall, 167 patients were included in the study, and intensive care unit mortality was 34.7%. Multivariate analysis indicated that antiretroviral therapy adherence and the Simplified Acute Physiology 3 score were independently related to hospital mortality. antiretroviral therapy adherence was a protective factor (OR 0.2; 95% CI 0.05–0.71; P = 0.01), and Simplified Acute Physiology 3 (OR 1.04; 95% CI 1.01–1.08; P < 0.01) was associated with increased hospital mortality. Conclusion Non-adherence to antiretroviral therapy is associated with hospital mortality in this population. Highly active antiretroviral therapy non-adherence may be associated with other comorbidities that may be associated with a worst prognosis in this scenario.

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