Archive for December 4, 2005

MAJOR ARTICLE – The Influence of Chronic Illnesses on the Incidence of Invasive Pneumococcal Disease in Adults

Source: The Journal of Infectious Diseases 2005;192:377-386

Moe H. Kyaw,1 Charles E. Rose, Jr.,1,a Alicia M. Fry,1,a James A. Singleton,2 Zack Moore,1,a Elizabeth R. Zell,1 and Cynthia G. Whitney,1 for the Active Bacterial Core Surveillance Program of the Emerging Infections Program Networkb

1Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, and 2Epidemiology and Surveillance Division, National Immunization Program, Centers for Disease Control and Prevention, Atlanta, Georgia

Pneumococcal disease is more frequent and more deadly in persons with certain comorbidities. We used 1999 and 2000 data from the Active Bacterial Core surveillance (ABCs) and the National Health Interview Survey (NHIS) to determine rates of invasive pneumococcal disease in healthy adults (18 years old) and in adults with various high-risk conditions. The risks of invasive pneumococcal disease in persons with specific chronic illnesses was compared with that in healthy adults, controlling for age, race, and the other chronic illnesses. Overall incidence rates, in cases/100,000 persons, were 8.8 in healthy adults, 51.4 in adults with diabetes, 62.9 in adults with chronic lung disease, 93.7 in adults with chronic heart disease, and 100.4 in adults who abused alcohol. Among the high-risk groups evaluated, risk was highest in adults with solid cancer (300.4), HIV/AIDS (422.9), and hematological cancer (503.1). Incidence rates increased with advancing age in adults with chronic lung disease, diabetes, and solid cancer. Black adults had higher incidence rates than white adults, both in healthy adults and in adults with chronic illnesses. These data support recommendations to provide pneumococcal vaccine to persons in these at-risk groups and underscore the need for better prevention strategies for immunocompromised persons.
Presented in part: 4th International Symposium on Pneumococci and Pneumococcal Diseases, Helsinki, Finland, 913 May 2004 (abstract EPI-44).
Financial support: Emerging Infections Program, Centers for Disease Control and Prevention.
Potential conflicts of interest: none reported.
a Present affiliations: Bacterial Vaccine Prevention Diseases Branch (C.E.R.) and Viral Vaccine Preventable Diseases Branch (Z.M.), National Immunization Program, and Division of Viral and Rickettsial Diseases (A.M.F.), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia.
b Team members are listed after the text.


December 4, 2005 at 9:41 pm Leave a comment

MAJOR ARTICLE – Highly Active Antiretroviral Therapy Started during Pregnancy or Postpartum Suppresses HIV-1 RNA, but Not DNA, in Breast Milk

Source: The Journal of Infectious Diseases 2005;192:713-719

Roger L. Shapiro,1,4 Thumbi Ndung’u,1 Shahin Lockman,1,3 Laura M. Smeaton,2 Ibou Thior,1 Carolyn Wester,1 Lisa Stevens,1 Gaseene Sebetso,5 Simani Gaseitsiwe,5 Trevor Peter,1 and Max Essex1

1Department of Immunology and Infectious Diseases and 2Center for Biostatistics in AIDS Research, Harvard School of Public Health, 3Infectious Disease Unit, Brigham and Women’s Hospital, and 4Division of Infectious Diseases, Beth Israel Deaconess Medical Center, Boston, Massachusetts; 5BotswanaHarvard School of Public Health AIDS Initiative Partnership for HIV Research and Education, Bontleng, Gaborone, Botswana

Background. The ability of highly active antiretroviral therapy (HAART) to reduce human immunodeficiency virus type 1 (HIV-1) RNA and DNA in breast milk has not been described.

Methods. We compared breast-milk HIV-1 RNA and DNA loads of women in Botswana who received HAART (nevirapine, lamivudine, and zidovudine) and women who did not receive HAART.

Results. Women in the HAART group received treatment for a median of 98 days (range, 67222 days) at the time of breast-milk sampling; 23 (88%) of 26 had whole breast-milk HIV-1 RNA loads Conclusions. HAART suppressed cell-free HIV-1 RNA in breast milk and may therefore reduce mother-to-child transmission (MTCT) of HIV-1 via breast-feeding. However, HAART initiated during pregnancy or early after delivery had no apparent effect on cell-associated HIV-1 DNA loads in breast milk. Clinical trials to determine MTCT among breast-feeding women receiving HAART are needed.

Presented in part: 12th Conference on Retroviruses and Opportunistic Infections, Boston, 2225 February 2005 (poster 793b).
Potential conflicts of interest: none reported.
Financial support: National Institutes of Childhood Health Development (grants R01-HD37793 and K23-HD01330).

December 4, 2005 at 9:38 pm Leave a comment

BRIEF REPORT – Reemergence of Hepatitis C Virus after 8.5 Years in a Patient with Hypogammaglobulinemia: Evidence for an Occult Viral Reservoir

Source: The Journal of Infectious Diseases 2005;192:1088-1092

William M. Lee,1 Julie E. Polson,1 D. Spencer Carney,1 Bogachan Sahin,2 and Michael Gale, Jr.2

1Department of Internal Medicine, Division of Digestive and Liver Diseases, and 2Department of Microbiology, University of Texas Southwestern Medical Center, Dallas

The question of whether viruses persist after apparent clearance of infection remains unanswered. Here, we describe a patient with hypogammaglobulinemia whose acute hepatitis C virus (HCV) infection appeared to resolve after receipt of interferon therapy, relapse immediately, and then clear spontaneouslyonly to relapse after receipt of corticosteroid therapy, and clear again, 8.5 years later. Sequencing indicated that the viruses detected during each relapse were virtually identical, with the hypervariable region 1 of E2 appearing to be monoclonal, which is typical of patients with hypogammaglobulinemia. Nonstructural 5A sequences exhibited quasispecies diversity initially but, after 8.5 years, had become monoclonal. The prolonged period of negativity for HCV RNA followed by relapse suggests that HCV may persist in apparent sustained viral responders.
Potential conflicts of interest: none reported.
Financial support: National Institutes of Health (grant AI48235 to M.G.); the Jeanne Roberts and the Rollin W. and Mary Ella King Funds of the Southwestern Medical Foundation, Dallas, Texas (to W.M.L.).


December 4, 2005 at 9:35 pm Leave a comment

MAJOR ARTICLE – Influence of Hepatitis C Virus Infection on HIV-1 Disease Progression and Response to Highly Active Antiretroviral Therapy

Source: The Journal of Infectious Diseases 2005;192:992-1002

Jürgen K. Rockstroh,1 Amanda Mocroft,2 Vincent Soriano,3 Cristina Tural,4 Marcello H. Losso,5 Andrzej Horban,6 Ole Kirk,7 Andrew Phillips,2 Bruno Ledergerber,8 and Jens Lundgren,7 for the EuroSIDA Study Groupa

1Department of Medicine I, University Hospital Bonn, Bonn, Germany; 2Royal Free Centre for HIV Medicine and Department of Primary Care and Population Sciences, Royal Free and University College Medical School, London, United Kingdom; 3Service of Infectious Diseases and Hepatology Unit, Hospital Carlos III, Madrid, and 4HIV Clinical Unit and IrsiCaixa Retrovirology Laboratory, Hospital Universitari Germans Trias Pujol, Universitat Autónoma de Barcelona, Badalona, Spain; 5Hospital Jose Maria Ramos Mejía, Buenos Aires, Argentina; 6Centrum Diagnostyki i Terapii AIDS, Warsaw, Poland; 7EuroSIDA Coordinating Centre, Copenhagen HIV-Programme, Hvidovre University Hospital, Copenhagen, Denmark; 8University Hospital, Zurich, Switzerland

Objective. To assess hepatitis C virus (HCV) antibody prevalence in the EuroSIDA cohort, along with survival, human immunodeficiency virus (HIV)1 disease progression, virologic response (plasma HIV-1 RNA load of Results. HCV serostatus at or before enrollment was available for 5957 patients; 1960 (33%) and 3997 (67%) were HCV seropositive and seronegative, respectively. No association between an increased incidence of acquired immunodeficiency syndrome-defining illnesses or death and HCV serostatus was seen after adjustment for other prognostic risk factors known at baseline (adjusted incidence rate ratio [IRR], 0.97 [95% confidence interval {CI}, 0.811.16]). However, there was a large increase in the incidence of liver diseaserelated deaths in HCV-seropositive patients in adjusted models (IRR, 11.71 [95% CI, 6.4221.34]). Among 2260 patients of known HCV serostatus initiating HAART, after adjustment, there was no significant difference between HCV-seropositive and -seronegative patients with respect to virologic response (relative hazard [RH], 1.13 [95% CI, 0.841.51]) and immunologic response, whether measured as a 50% increase (RH, 0.94 [95% CI, 0.771.16]) or a 50 cells/L increase (RH, 0.92 [95% CI, 0.771.11]) in CD4 cell count after HAART initiation.

Conclusions. HCV serostatus did not affect the risk of HIV-1 disease progression, but the risk of liver disease-related deaths was markedly increased in HCV-seropositive patients. The overall virologic and immunologic responses to HAART were not affected by HCV serostatus.

Presented in part: 11th Conference on Retroviruses and Opportunistic Infections, San Francisco, 811 February 2004 (poster 799).
Potential conflicts of interest: J.K.R. has received consultation or lecture fees from Abbott, Boehringer-Ingelheim, Bristol-Myers Squibb, Gilead, GlaxoSmithKline, Roche, and Schering-Plough. B.L. has received travel grants from Roche, Abbott, Bristol-Myers Squibb, GlaxoSmithKline, Merck Sharp & Dohme, and Aventis. All other authors have reported no conflicts of interest.
Financial support: European Commission BIOMED 1 (grant CT94-1637), BIOMED 2 (grant CT97-2713), and Fifth Framework (grant QLK2-2000-00773) Programs; Bristol-Myers Squibb, GlaxoSmithKline, Roche, and Boehringer-Ingelheim (unrestricted grants); Swiss Federal Office for Education and Science (grant for the participation of Swiss centers).
a Study group members are listed after the text.

December 4, 2005 at 9:32 pm Leave a comment

MAJOR ARTICLE – Prevalence of Drug-Resistant HIV-1 Variants in Untreated Individuals in Europe: Implications for Clinical Management

Source: The Journal of Infectious Diseases 2005;192:958-966

Annemarie M. J. Wensing,1,2 David A. van de Vijver,1 Gioacchino Angarano,4 Birgitta Åsjö,9 Claudia Balotta,5 Enzo Boeri,6 Ricardo Camacho,11 Maire-Laure Chaix,12 Dominique Costagliola,13 Andrea De Luca,7 Inge Derdelinckx,15 Zehava Grossman,16 Osamah Hamouda,18 Angelos Hatzakis,19 Robert Hemmer,20 Andy Hoepelman,2 Andrzej Horban,21 Klaus Korn,17 Claudia Kücherer,18 Thomas Leitner,22 Clive Loveday,23 Eilidh MacRae,23 Irina Maljkovic,24 Carmen de Mendoza,25 Laurence Meyer,14 Claus Nielsen,31 Eline L. Op de Coul,3 Vidar Ormaasen,10 Dimitris Paraskevis,19 Luc Perrin,26 Elisabeth Puchhammer-Stöckl,27 Lidia Ruiz,28 Mika Salminen,29 Jean-Claude Schmit,20 Francois Schneider,20 Rob Schuurman,1 Vincent Soriano,25 Grzegorz Stanczak,21 Maja Stanojevic,30 Anne-Mieke Vandamme,15 Kristel Van Laethem,15 Michela Violin,5 Karin Wilbe,24 Sabine Yerly,26 Maurizio Zazzi,8 and Charles A. Boucher,1 for the SPREAD Programmea

Background. Infection with drug-resistant human immunodeficiency virus type 1 (HIV-1) can impair the response to combination therapy. Widespread transmission of drug-resistant variants has the disturbing potential of limiting future therapy options and affecting the efficacy of postexposure prophylaxis.

Methods. We determined the baseline rate of drug resistance in 2208 therapy-naive patients recently and chronically infected with HIV-1 from 19 European countries during 19962002.

Results. In Europe, 1 of 10 antiretroviral-naive patients carried viruses with 1 drug-resistance mutation. Recently infected patients harbored resistant variants more often than did chronically infected patients (13.5% vs. 8.7%; P = .006). Non-B viruses (30%) less frequently carried resistance mutations than did subtype B viruses (4.8% vs. 12.9%; P Conclusions. Drug-resistant variants are frequently present in both recently and chronically infected therapy-naive patients. Drug-resistant variants are most commonly seen in patients infected with subtype B virus, probably because of longer exposure of these viruses to drugs. However, an increase in baseline resistance in non-B viruses is observed. These data argue for testing all drug-naive patients and are of relevance when guidelines for management of postexposure prophylaxis and first-line therapy are updated.

Financial support: European Commission (SPREAD-programme QLK2-CT-2001-01344); Istituto Superiore di SanitàProgetto AIDS (grants 39C.7 and 40D.07 to G.A.); Norwegian health authorities (to B.Å. for resistance analysis); Italian Institute of Health (grants 2000 30D.55 and 30D.06 to C.B. and M.V.); Agence Nationale de Recherches sur le SIDA; Istituto Superiore di SanitàProgetto Nazionale AIDS I-IV (to A.d.L.); Ricerca Corrente degli IRCCS 2003 (to A.d.L.); Fondi Ateneo Università Cattolica S Cuore (to A.d.L.); German Federal Ministry of Health and Social Affairs (grant 325-4476-02/3); German Federal Ministry of Education and Research, Competence Network on HIV/AIDS (grant 01Kl0212); National Institutes of Health and US Department of Energy (contract Y1A11500 to T.L.); Red de Investigacion en SIDA (project 173 to C.L.); Fundacion Investigacion y Educacion en SIDA; Abbott Diagnostics (genotyping kits); Swiss National Research Foundation (grant 3345-64120.00 to S.Y.); Swiss HIV Cohort Study (grant 3345-062041 to S.Y.); Red Tematica Cooperativa de Investigacion en SIDA (Red de Grupos 173) del FISss; AIDS Reference Laboratory of Leuven, which receives support from the Belgian Ministry of Social Affairs, Health Insurance System (to A.V.); V Programma AIDS, Ministero della Sanita, Rome (grant 30F.52 to M.Z.). 
Potential conflicts of interest: D.v.d.V., B.Å., C.B., E.B., M.-L.C., I.D., Z.G., O.H. R.H., A. Hoepelman, C.K., T.L., E.M., I.M., C.M., L.M., C.N., E.O.d.C., V.O., D.P., L.P., E.P.-S., L.R., M. Salminen, J.-C.S., F.S., R.S., V.S., G.S., M. Stanojevic, A.V., K.V.L., M.V., K.W.R., and S.Y., none. A.W. has served as a temporary adviser for Abbot, Bristol-Myers Squibb, and GlaxoSmithKline. G.A. is an advisory board member of Boehringer Ingelheim Italia, Bristol-Myers Squibb Italia, and Gilead Italia. R.C. is a medical adviser for Boehringer-Ingelheim Portugal. D.C. has received consultancy fees, grant support, and support for conference attendance from pharmaceutical companies including GlaxoSmithKline, Roche, Abbott, Bristol Myers Squibb, and Boehringer Ingelheim. A.d.L. has served as consultant or has been member of advisory boards for GlaxoSmithKline and Bayer Diagnostics. A. Hatzakis has been consultant to Schering-Plough, Gilead Sciences, and Bayer; has received research support from Schering-Plough, Gilead Sciences, Roche Molecular Systems, Chiron, Bayer, and Celera; and has participated in advisory boards of Gilead Sciences, Abbott Diagnostics, Bayer, and Idenix. A. Horban is a member of an advisory board for Abbott Virology. K.K. has received honoraria from and/or participated in ad hoc advisory boards for Abbott, Bayer, Bristol-Myers Squibb, GlaxoSmithKline, and Roche. C.L. is the director of the ICVC Charitable Trust, which receives or has received grants from Bayer Diagnostics, Roche Diagnostics, VGI, Boerinhger Ingelheim, Abbott, GlaxoSmithKline, BMS, MRC, the European Union, and public voluntary contributions, and currently serves as an expert adviser to the Bayer Diagnostics Resistance Panel and the GlaxoSmithKline Expert Panel. C.A.B.B. has served as a short-term consultant to Roche Finland and BMS Finland. M.Z. has received research support from GlaxoSmithKline, Bristol-Myers Squibb, Gilead, and the Abbott Molecular Diagnostics Speakers Bureau and has served as consultant for GlaxoSmithKline, Bristol-Myers Squibb, and Abbott Molecular Diagnostics. C.B. serves as an expert adviser to Roche, Abbot, GlaxoSmithKline, Bristol-Myers Squibb, and Boehringer Ingelheim.
a Author affiliations are listed after the text.

December 4, 2005 at 9:29 pm Leave a comment

MAJOR ARTICLE – CD4 Lymphocyte Percentage Predicts Disease Progression in HIV-Infected Patients Initiating Highly Active Antiretroviral Therapy with CD4 Lymphocyte Counts >350 Lymphocytes/mm3

Source: The Journal of Infectious Diseases    2005;192:950-957

Todd Hulgan,1,2 Stephen Raffanti,1,4 Asghar Kheshti,4 Robert B. Blackwell,4 Peter F. Rebeiro,1 Gema Barkanic,1 Brandon Ritz,3 and Timothy R. Sterling1,2

1Department of Medicine, Division of Infectious Diseases, and 2Center for Health Services Research, 3Vanderbilt University School of Medicine, and 4Comprehensive Care Center, Nashville, Tennessee

Background. The optimal timing of highly active antiretroviral therapy (HAART) in human immunodeficiency virus (HIV)infected patients with 200 absolute CD4 lymphocytes/mm3 is unknown. CD4 lymphocyte percentage could add prognostic information.

Methods. Persons who initiated HAART between 1 January 1998 and 1 January 2003, received 30 days of therapy, and had baseline CD4 lymphocyte data available were included in the study. The log-rank test for time to event and Cox proportional hazards models were used to determine predictors of a new acquired immunodeficiency syndromedefining illness or death.

Results. A total of 788 patients met the inclusion criteria. At baseline, subjects had a median of 225 CD4 lymphocytes/mm3 and 17% CD4 lymphocytes. Subjects with 350 absolute CD4 lymphocytes/mm3 at baseline (P = .03). CD4 lymphocyte percentage Conclusions. In this cohort, CD4 lymphocyte percentage predicted disease progression in HIV-infected subjects who initiated therapy with >350 CD4 lymphocytes/mm3. This information may help identify persons who will derive the greatest benefit from initiation of HAART.

Potential conflicts of interest: none reported.
Financial support: Vanderbilt Clinical Research Scholars Award (grant K12 RR17697 to T.H.); National Institute of Allergy and Infectious Diseases (grant K23 AI01654 to T.R.S.); Vanderbilt-Meharry Center for AIDS Research (National Institutes of Health program P30 AI 54999).


December 4, 2005 at 9:26 pm Leave a comment

PERSPECTIVE – HIV Superinfection

Source: The Journal of Infectious Diseases 2005;192:438-444

Davey M. Smith,1 Douglas D. Richman,1,2 and Susan J. Little1

1University of California, San Diego, and 2Veterans Affairs San Diego Healthcare System, San Diego

Worldwide, 16 cases of HIV-1 superinfection in humans have been reported since 2002. Superinfection is defined as the reinfection of an individual who already has an established infection with a heterologous HIV strain. Controversy exists surrounding superinfection, because it has implications concerning our understanding of worldwide HIV diversity, individual immunity and disease progression, and vaccine development. Here, we review the current understanding of HIV superinfection.
Financial support: AIDS Clinical Trials Group (ACTG), funded by the National Institute of Allergy and Infectious Diseases (grants 5K23AI055276, AI27670, and AI043638); ACTG Central Group Grant (U01AI38858); University of California, San Diego, Center for AIDS Research (grant AI 36214); National Institutes of Health (grants AI29164 and AI047745); Research Center for AIDS and HIV Infection, Veterans Affairs San Diego Healthcare System.

December 4, 2005 at 9:23 pm Leave a comment

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