Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Correspondence AIDS 2009, 23:869–873 Maraviroc and CD4 R cell count recovery in patients with virologic suppression and blunted CD4 R cell response We wish to comment on the recent Editorial review on maraviroc by Soriano et al. [1]. Their suggestion that the drug could be used for managing the subset of patients unable to show an adequate CD4 cell recovery despite achieving sustained virological suppression with highly- active antiretroviral therapy (HAART) [1] has been tested in a recent nonrandomized, prospective, open-label, proof-of-concept pilot study with a minimum follow-up of 150 days, where maraviroc 300mg was added to an ongoing HAART regimen in nine HIV-infected indi- viduals on stable HAART with HIV-1 RNA less than 50 copies/ml for at least 1 year and a stable CD4 þ cell count of less than 250 cells/mm 3 [2]. Although two patients showed dramatic increases in CD4 cell counts (þ112 and þ130), the average change was þ14 cells for all patients, and was not statistically significant (P > 0.39). Obviously, further studies with a longer follow-up will be required to eventually demonstrate a significant effect of maraviroc. Importantly, Soriano et al. [1] failed to discuss possible drawbacks of maraviroc use in certain HIV-infected individuals. A significant increase in CCR5D32 allele prevalence has been found in patients with tickborne encephalitis (TBE, an often fatal infection caused by the TBE virus, TBEV), compared with that in patients with non-TBE aseptic meningoencephalitis and in healthy control individuals seronegative for TBEV [3]. In addi- tion, functional CCR5 seems to be required to prevent symptomatic disease after infection with West Nile virus (WNV), an RNA flavivirus that can cause neuroinvasive disease, particularly in patients with impaired cellular immunity [4]. Indeed CCR5 is specifically required for central nervous system leukocyte trafficking for the purpose of viral clearance, as shown in mouse models [5]. We think that attention needs to be drawn to this possible caveat of maraviroc use, considering the diffusion of TBEV in Eastern Europe, a region where HIV infection is still on the rise, and of WNV in USA. Acknowledgements None of the authors have any conflict of interest. Massimiliano Lanzafame, Emanuela Lattuada and Sandro Vento contributed to the concept and writing of the article. All authors have read and approved the text. Massimiliano Lanzafame a , Emanuela Lattuada a and Sandro Vento b , a Unit of Infectious Diseases, ‘G.B. Rossi’ Hospital,Verona, and b Unit of Infectious Dis- eases, ‘Annunziata’ Hospital, Cosenza, Italy. Correspondence to Massimiliano Lanzafame, via strada romana 11, San Bonifacio (Verona), CAP 37047, Italy. Tel: +39 0458128256; fax: +39 0458128257; e-mail: masino69@hotmail.com Received: 5 December 2008; accepted: 11 December 2008. References 1. Soriano V, Geretti AM, Perno CF, Fatkenheuer G, Pillay D, Reynes J, et al. Optimal use of maraviroc in clinical practice. AIDS 2008; 22:2231–2240. 2. Eng RHK, Perez G, Paez SL, Chiang TS, Smith SM. Impact of adding maraviroc to HIV patients with undetectable plasma RNA but are non-CD4 progressors (CD4  200 cell/mm 3 ) [abstract H-1247]. In: 48th Annual ICAAC/IDSA 46th Annual Meeting; 25–28 October 2008; Washington, DC; 2008. 3. Kindberg E, Mickiene A, Ax C, A ˚ kerlind B, Vene S, Lindquist L, et al. A deletion in the chemokine receptor 5 (CCR5) gene is associated with tickborne encephalitis. J Infect Dis 2008; 197: 266–269. 4. Lim JK, Louie CY, Glaser C, Jean C, Johnson B, Johnson H, et al. Genetic deficiency of chemokine receptor CCR5 is a strong risk factor for symptomatic West Nile virus infection: a meta- analysis of 4 cohorts in the US epidemic. J Infect Dis 2008; 197:262–265. 5. Klein RS. A moving target: the multiple roles of CCR5 in infectious diseases. J Infect Dis 2008; 197:183–186. DOI:10.1097/QAD.0b013e3283262aa0 Etravirine–raltegravir, a marked interaction in HIV-1-infected patients: about four cases Recently, new compounds, capable of overcoming the extensive class resistances observed in multitreated patients, became available for HIV-infected patients. Raltegravir (RAL) is the first compound of a new class of antiretrovirals, the integrase inhibitors. Etravirine (ETV), a next-generation nonnucleoside reverse transcriptase inhibitor (NNRTI), has been demonstrated to be active against HIV strains presenting resistance to first- generation NNRTI. ETV and RAL are both extensively metabolized, mainly by cytochrome P450-3A (CYP3A) for ETV and by ISSN 0269-9370 Q 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins 869