HIV-2 viral tropism influences CD4+ T cell count regardless of viral load.
BACKGROUND
HIV-2 infection is characterized by low plasma viraemia and slower progression to AIDS in comparison with HIV-1 infection. However, antiretroviral therapy in patients with HIV-2 is less effective and often fails to provide optimal CD4 recovery.


METHODS
We examined viral tropism in persons with HIV-2 infection enrolled in the HIV-2 Spanish cohort. Viral tropism was estimated based on V3 sequences obtained from plasma RNA and/or proviral DNA.


RESULTS
From a total of 279 individuals with HIV-2 infection recorded in the Spanish national register, 58 V3 sequences belonging to 42 individuals were evaluated. X4 viruses were recognized in 14 patients (33%). Patients with X4 viruses had lower median CD4+ cell counts than patients with R5 viruses [130 (17-210) versus 359 (180-470) cells/mm(3); P = 0.007]. This was true even considering only the subset of 19 patients on antiretroviral therapy [94 (16-147) versus 184 (43-368) cells/mm(3); P = 0.041]. In multivariate analysis, significant differences in CD4+ cell counts between patients with X4 and R5 viruses remained after adjusting for age, gender, antiretroviral therapy and viral load.


CONCLUSIONS
The presence of X4-tropic viruses in HIV-2 infection is associated with low CD4+ cell counts, regardless of antiretroviral treatment. Along with CD4+ cell counts, viral tropism testing may assist decisions about when to initiate antiretroviral therapy in HIV-2-infected individuals.
Hospital Carlos III, Madrid, Spain ana.trevino.rc@gmail.com.
Ana
A
Treviño
Hospital Carlos III, Madrid, Spain.
Vicente
V
Soriano
Division of Clinical Virology, INIBIC-Complejo Hospitalario Universitario de A Coruña, A Coruña, Spain.
Eva
E
Poveda
Hospital Carlos III, Madrid, Spain.
Patricia
P
Parra
Hospital de Poniente, Almería, Spain.
Teresa
T
Cabezas
Hospital Vall d'Hebron, Barcelona, Spain.
Estrella
E
Caballero
Hospital Miguel Servet, Zaragoza, Spain.
Lourdes
L
Roc
Centro Sanitario Sandoval, Madrid, Spain.
Carmen
C
Rodríguez
Hospital Rio Hortega, Valladolid, Spain.
Jose M
JM
Eiros
Hospital Carlos III, Madrid, Spain.
Mariola
M
Lopez
Hospital Carlos III, Madrid, Spain Hospital Universitario Puerta de Hierro, Majadahonda, Madrid, Spain.
Carmen
C
De Mendoza
D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D065100:CCR5 Receptor Antagonists / Q000627:therapeutic use; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D003510:Cyclohexanes / Q000627:therapeutic use; D005260:Female; D015699:HIV Envelope Protein gp120 / Q000097:blood; D023581:HIV Fusion Inhibitors / Q000627:therapeutic use; D015658:HIV Infections / Q000097:blood / Q000188:drug therapy / Q000276:immunology*; D015498:HIV-2 / Q000145:classification / Q000276:immunology / Q000502:physiology*; D006801:Humans; D008297:Male; D000077592:Maraviroc; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D012367:RNA, Viral / Q000097:blood; D013030:Spain; D014230:Triazoles / Q000627:therapeutic use; D019562:Viral Load; D056189:Viral Tropism / Q000276:immunology / Q000502:physiology*; D014766:Viremia / Q000097:blood
D019380:Anti-HIV Agents; D065100:CCR5 Receptor Antagonists; D003510:Cyclohexanes; D015699:HIV Envelope Protein gp120; D023581:HIV Fusion Inhibitors; C059762:HIV envelope protein gp120 (305-321); D010446:Peptide Fragments; D012367:RNA, Viral; D014230:Triazoles; D000077592:Maraviroc
CCR5 antagonists; maraviroc; proviral load