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. 2005 Mar;79(5):2823–2830. doi: 10.1128/JVI.79.5.2823-2830.2005

TABLE 3.

Time points of first detection of T-cell and antibody-mediated antiviral activity following infection

Patient Time point (DFOSx) Viral load (RNA copies/ml) Anti-HIV antibodiesa Anti-gp120 antibodies (reciprocal end point titer)b T-cell activityc,d CMId,e NAbd,f
MM4 17 160,000 + 100 NDg +
206 30,200 12,800 +
MM8 12 5,927,000 + <100 + +
81 41,900 3,200 +
MM19 13 5,678,900 + <100 + +
519 371,700 12,800
MM22 14 8,311,000 + 100 + ND ND
MM23 9 11,105,300 + <100 + +
204 117,600 51,200 +
MM27 28 353,200 + 800 + +
466 10,600 12,800 +
MM28 6 4,337,100 + 100 + +
503 38,600 102,400
a

All patients had detectable levels of anti-HIV antibodies from the first study sample in diagnostic tests (Murex HIV-1.2.0; Abbott, Wiesbaden, Germany; Wellcozyme HIV Recombinant; Abbott; Serodia HIV-1/2; Fujirebio Inc., Tokyo, Japan; and VIDAS HIV Duo; bioMérieux, Marcy L’Etoile, France).

b

The titer of anti-gp120 antibodies in patient sera was determined by an in-house enzyme-linked immunosorbent assay as described in Material and Methods; the lowest serum dilution tested was 1:100.

c

HIV-specific T-cell responses were detected in recombinant vaccinia virus-based IFN-γ ELISPOT assays (Table 2).

d

+, detectable response; −, undetectable response.

e

The antibody-dependent complement-mediated virus inactivation was intermediate (approximately 50% inactivation of input virus) in early sera from patients MM23, MM27, and MM28 and was strong (approximately 90% inactivation of input virus) in early sera from patients MM4, MM8, and MM19.

f

Neutralization defined as ≥90% reduction of infection of input virus (Table 1).

g

ND, not determined, as no (suitable) samples were available for analysis.