Is total lymphocyte count a reliable predictor of the CD4 lymphocyte cell count in resource-limited settings?
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INTRODUCTION: To assess the factors associated with progression of infection and death in HIV-positive patients with severe immunodepression in the era of highly active antiretroviral therapy (HAART). METHODS: We studied 146 HIV-infected patients with < 100 x 10(6)/L CD4+ lymphocytes and positive cytomegalovirus (CMV) serology enrolled between December 1997 and October 1998 and prospectively followed a median of 12.1 months. The main outcome measures were progression of HIV infection, defined as the appearance of a new AIDS-defining disease (CDC category C) or death. HIV viral load, lymphocyte count (CD4+ and CD8+), HAART administration and other clinical variables were evaluated at baseline. CMV viremia (determined by PCR) and HAART efficacy were recorded during follow-up. RESULTS: Progression was observed in 40% of patients and 17% died. Factors associated with progression or death were CD4+ lymphocyte count less than 50 x 10(6)/L, CD8+ lymphocyte count less than 500 x 10(6)/L, HIV viral load more than 300,000 copies RNA/mL, CMV viremia, and absence or inefficacy of HAART. In the multivariate model, absence of HAART and low CD4+ and CD8+ counts remained statistically associated with progression, but the only variable associated with death was CMV viremia. CONCLUSIONS: In patients with advanced HIV infection, CD4+ and CD8+ cell count and HAART were the most important factors related to progression, and CMV viremia was the strongest predictor of death.
OBJECTIVE: To study the prognostic role of pregnancy on the progression of human immunodeficiency virus (HIV) infection. METHODS: In a prospective cohort study at the Bordeaux University Hospital, France, 57 women who completed a pregnancy during the course of their HIV infection were compared with 114 HIV-infected women who never conceived. The two groups were matched on CD4 lymphocyte count (CD4), age, and year of HIV diagnosis. The main outcome measures were death, occurrence of a first AIDS-defining event, and drop of the CD4 below 200/mm3. RESULTS: The mean follow-up period in pregnant women was 61 months from HIV diagnosis (median CD4 at entry 455/mm3) and 54 months from beginning of pregnancy. Nonpregnant women were followed-up for 50 months since HIV diagnosis (median CD4 460/mm3). The proportion of asymptomatic women at entry in the study was 51 of 57 (90%) in pregnant and 87 of 114 (76%) in nonpregnant women. No significant difference was observed between the two groups with regard to the different end points studied, even after adjustment for other prognostic variables. Adjusted hazard ratios (pregnant/nonpregnant) were 0.92 for death (95% confidence interval [CI] 0.40-2.12), 1.02 for occurrence of a first AIDS-defining event (95% CI 0.48-2.18), and 1.20 for drop of the CD4 to less than 200/mm3 (95% CI 0.63-2.27). CONCLUSION: In a cohort of HIV-infected women with mild to moderate immunosuppression, pregnancy did not accelerate progression to AIDS or death.
The Dynabeads method showed the potential for enumerating CD4 T lymphocytes (CD4 count) in HIV-1-infected individuals. The large volume of Dynabeads required for 1 sample and complex procedure made the method expensive and not easy for use, however. To decrease the cost and simplify the procedure, we reduced the volume of the Dynabeads, added wash times, and skipped over the staining step so as to count the CD4 cells directly under an optical microscope. The CD4 count of 246 blood samples using our modified Dynabeads method (DynabeadsCD4) showed a significant correlation with that obtained by flow cytometry (FlowcytoCD4) (r = 0.91 [P < 0.0001]; slope = 1.03, intercept = -16). The sensitivity and specificity for a CD4 count less than 200 cells/microL were 79% and 94%, and for a CD4 count less than 350 cells/microL, the sensitivity and specificity were 95% and 88%, respectively. The positive and negative predictive values for a CD4 count less than 350 cells/microL were 97% and 83%, respectively. The systematic error was 8 cells/microL (95% confidence interval [CI]: 0.4-16). The cost of Dynabeads for 1 sample was less than $1.00; thus, the estimated cost per DynabeadsCD4 test is less than $3.00, including the cost of other disposable materials. Our modified method is simple, economic, and accurate enough to monitor antiretroviral therapy in resource-limited situations.
BACKGROUND: Lymphopenia is frequently observed in patients with cancer and correlates with the risk of febrile neutropenia and early death after chemotherapy. The phenotype of the depleted lymphocyte populations was investigated in the current study. METHODS: Peripheral blood lymphocyte subsets (CD3, CD4, CD8, CD19, CD56) were quantified on Day 1 using fluorescence-activated cell sorting in a prospective study of 213 patients with cancer treated with chemotherapy in a single oncology ward during 12 months. Correlations between lymphocyte phenotype, clinical characteristics, and the risk of febrile neutropenia and early death within 31 days after chemotherapy were investigated in univariate and multivariate analyses. RESULTS: Total lymphocyte count and CD3, CD4, and CD8 lymphocyte subsets were significantly lower in patients who experienced febrile neutropenia. Total lymphocyte count and CD3, CD4, CD8, CD19, and CD56 lymphocyte subsets were significantly lower in patients who died within 31 days after chemotherapy. Using logistic regression, CD4 lymphopenia (< 450/muL; odds ratio [OR] = 2.9, 95% confidence interval [CI] = 1.5-5.9) and the dose of chemotherapy (OR = 3,9, 95% CI = 2.0-7.8) were both identified as independent risk factors for febrile neutropenia. Fifty-four percent of patients with both risk factors experienced febrile neutropenia. CD4 lymphocyte count < 450/muL was also an independent risk factor for early death (OR = 7.7, 95% CI = 1.7-35). Thirteen percent of patients with a CD4 lymphocyte count </= 450/muL died within 31 days after chemotherapy. Eighty-seven percent (14 of 16) of patients who died before Day 31 had a CD4 lymphocyte count < 450/muL. CONCLUSIONS: A low CD4 count was an independent risk factor for febrile neutropenia and early death in patients receiving cytotoxic chemotherapy.
BACKGROUND: The beta-chemokine receptor CCR-5 is the coreceptor for cellular entry by non-syncytium-inducing (NSI) HIV-1 strains that dominate early in infection. A 32 base-pair deletion (delta32) in the CCR-5 gene renders this coreceptor non-functional. Heterozygosity for this deletion [delta32/wild-type (wt)] is associated with slow disease progression. The purpose of this study was to document the combined impact on HIV-1 disease progression of the CCR-5 genotype and the biological phenotype of HIV-1. METHODS: In a cross-sectional study of 258 HIV-1-infected Swedish individuals, the CCR-5 genotype (wt/wt or delta32/wt) was determined by polymerase chain reaction and the biological phenotype [NSI or syncytium-inducing (SI)] of virus isolates was determined in the MT-2 cell assay. Clinical status, HIV-1 RNA levels in plasma, CD4+ lymphocyte counts, and rate of CD4+ lymphocyte decline, based on retrospective analysis of CD4+ lymphocyte counts, were also recorded. None of the individuals were treated with protease inhibitors. RESULTS: The prevalence of the delta32/wt genotype was 23%. Subjects with the delta32/wt CCR-5 genotype more often carried SI virus than subjects with the wt/wt genotype (49 versus 35%; P=0.067), but there were no differences between the two groups in prevalence of AIDS, viral load, CD4+ lymphocyte count or CD4+ slope. NSI virus isolates were found in 159 (62%) out of 258 individuals. Individuals with NSI had lower prevalence of AIDS (39 versus 19%; P < 0.01), higher CD4+ lymphocyte counts (289+/-188 x 10(6)/l versus 153+/-162 x 10(6)/l; P=0.001), lower viral loads (median, 4.45 log10 versus 4.91 log10 copies/ml; P < 0.01) and a lower prevalence of the delta32/wt genotype (19 versus 29%; P=0.067) compared with individuals with SI virus. When the material was further subdivided, subjects with the delta32/wt genotype and SI virus had the highest prevalence of AIDS (P < 0.001), lowest CD4+ lymphocyte count (P=0.0001) and highest viral load (P=0.023) whereas the opposite was true for subjects with the delta32/wt genotype and NSI virus. A significantly higher proportion of subjects with NSI virus with delta32/wt and wt/wt CCR-5 genotype had been immunized with recombinant gp160. CONCLUSION: In summary, the delta32/wt CCR-5 genotype has a protective effect against HIV-1 disease progression that appears to be limited to individuals carrying HIV-1 variants with NSI phenotype. Immunization with recombinant gp160 tended to reduce the frequency of SI phenotypes.
A case-control study was conducted at two institutions to determine whether the absolute CD4 lymphocyte count or the percentage of lymphocytes bearing the CD4 marker (i.e., the CD4 percentage) is a more accurate indicator of underlying immune status in splenectomized patients infected with human immunodeficiency virus (HIV). Each of nine splenectomized HIV-infected cases was matched with six nonsplenectomized HIV-infected controls--three matched for CD4 lymphocyte count and three for CD4 percentage. In analyses including the eight cases with an initial CD4 lymphocyte count of > 200/mm3, controlling for the CD4 count revealed differences between cases and controls in terms of CD4 percentage (range, 10%-41% and 17%-54%, respectively; P < .01) and Centers for Disease Control and Prevention (CDC) clinical stage (P = .06). Controlling for the CD4 percentage revealed a significant difference between cases and controls in terms of CD4 count (range, 396-1,040 and 55-784 cells/mm3, respectively; P < .01) but not CDC clinical stage (P > .7). These data suggest that the numerical relationship between the CD4 lymphocyte count and the CD4 percentage among splenectomized HIV-infected patients with more than 200 CD4 cells/mm3 differs from that among nonsplenectomized patients. The CD4 percentage appears to be a more accurate indicator of the underlying level of immune function in the former group of patients.
OBJECTIVE: To assess the ability of the CD8 lymphocyte count and immunoglobulin (Ig) A level, measured at the early stage of HIV infection when the CD4 lymphocyte count remains relatively high, to predict the future rate of CD4 lymphocyte loss and hence the risk of AIDS. DESIGN: Cohort of recently infected haemophiliacs with relatively high CD4 lymphocyte counts followed for up to 8.5 years from baseline measurement of CD8 lymphocyte counts and IgA levels. SETTING: A regional haemophilia centre based in a major teaching hospital. PATIENTS: Eighty-four of 111 patients with haemophilia who seroconverted to HIV between 1979 and 1985 in whom CD8 lymphocyte counts and IgA levels were measured soon after seroconversion (mean, 2.7 years; maximum, 5 years) while CD4 lymphocyte counts remained relatively high (median, 600 x 10(6)/l; minimum, 300 x 10(6)/l). OUTCOME MEASURES: Development of severe immunodeficiency defined by a CD4 lymphocyte count falling below 50 x 10(6)/l, and AIDS. RESULTS: Individuals with high CD8 counts (P < 0.008) and high IgA levels (P < 0.003) at baseline experienced a more rapid rate of CD4 lymphocyte loss than those with low baseline levels. A score was derived to combine the predictive ability of CD8 count and IgA level. Estimated proportions with CD4 counts below 50 x 10(6)/l after 8 years of follow-up were 100, 30 and 14% for those with high, intermediate and low baseline scores, respectively. The CD8/IgA score showed similar ability to predict the future occurrence of AIDS (P < 0.0001; log-rank test). CONCLUSION: Immune activation seen in HIV infection, as reflected by raised CD8 counts and IgA levels, appears to be linked to the process of CD4 lymphocyte depletion. Measurement of these markers in the years following infection, when CD4 lymphocyte counts remain high, provides a first indication of a patient's long-term prognosis.
INTRODUCTION: This study aims to evaluate the correlation and agreement between 2 methodologies of CD4 lymphocyte enumeration. MATERIALS AND METHODS: Fifty-two blood samples from patients with human immunodeficiency virus (HIV) infection were sent for CD4 lymphocyte enumeration at 2 major hospitals using dual-platform flow cytometry where the absolute lymphocyte counts were determined on separate haematology analyzers. CD4 cell enumeration was accomplished using 3-colour flow cytometry on the FACSCalibur cytometer (Becton Dickinson) in Hospital A and 4-colour flow cytometry on the Coulter Epic XL cytometer (Beckman Coulter) in Hospital B. The percentages and absolute counts of CD4 lymphocytes obtained were analysed using both linear regression and Bland-Altman plots. RESULTS: On linear regression plots, the total white cell counts, absolute lymphocyte counts, CD4 lymphocyte percentages and absolute CD4 counts from the 2 hospitals correlated well with correlation coefficients, r > 0.95. On the Bland-Altman plots, there was a mean difference of 0.13 x 10(9)/L and 0.06 x 10(9)/L in the total white cell and absolute lymphocyte counts from the 2 hospitals respectively. The CD4 lymphocyte percentages revealed a mean difference of only 0.05% (95% limits of agreement, -3.6 to 3.7%) but there was a mean difference of 14/uL in the absolute CD4 lymphocyte counts (95% limits of agreement, -113 to 142/uL). CONCLUSIONS: The CD4 lymphocyte percentages obtained using the 3-colour and 4-colour flow cytometry correlated and agreed well. However, the absolute CD4 lymphocyte counts obtained using the dual-platform technique in both the hospitals did not agree well. Hence, absolute CD4 lymphocyte counts from the 2 hospitals cannot be used interchangeably in clinical practice due to poor inter-laboratory comparability.
OBJECTIVE: To determine whether racial differences exist in the rate of CD4 lymphocyte decline in HIV-1-infected homosexual men. DESIGN: Prospective cohort study. STUDY POPULATION: Non-Hispanic white (n = 321) and black (n = 102) HIV-1-seropositive homosexual and bisexual men were recruited from the Baltimore/Washington, DC metropolitan areas between 1984-1985 and 1987-1990, and evaluated semiannually. MAIN MEASUREMENTS: Changes in CD4 lymphocyte count and CD4 percentage over time were analysed using linear regression methods for the 271 white and 69 black participants who had at least four semiannual CD4 lymphocyte measurements. RESULTS: Rate of decline in CD4 lymphocyte count over 6 months was much slower among black than white seroprevalent men at all levels of baseline CD4 count (baseline 201-400 x 10(6)/l: + 0.24 versus -17.7 x 10(6)/l; 401-600 x 10(6)/l: -11.3 versus -23.9 x 10(6)/l; 601-800 x 10(6)/l: -15.1 versus -35.2 x 10(6)/l; > 800 x 10(6)/l: -4.3 versus -42.7 x 10(6)/l for black versus white, respectively), although this was only statistically significant for the lowest and highest strata of baseline CD4 count. These racial differences persisted after adjustment for recruitment period (1984-1985 or 1987-1990), follow-up duration, age and zidovudine therapy or Pneumocystis carinii pneumonia prophylaxis. Similar findings were observed among the 70 white and 11 black seroconverters. Black participants were also less likely than a subgroup of white participants matched on baseline CD4 lymphocyte count to be HIV-1 p24 antigen-positive. However, after acid dissociation of samples initially p24 antigen-negative, there were no significant differences in the prevalence of p24 antigenemia at enrollment or after 1 year of follow-up. CONCLUSIONS: This analysis suggests a more gradual decline in CD4 lymphocyte count among black than white Americans. The clinical significance of and reasons for this are unclear, but the lower prevalence of p24 antigenemia due to immune complexing among black Americans suggests that racial differences in the immune response to HIV may exist. Additional studies are needed to validate these findings in a larger cohort of non-whites, and to assess their relationship with other measures of cell-mediated immune function.
Our objective was to evaluate the effect of intravenous immunoglobulin (IVIG) on absolute CD4+ lymphocyte count (CD4+ count) trends in human immunodeficiency virus- (HIV) infected children enrolled in a trial of IVIG for infection prophylaxis. To that end, we conducted a randomized, double-blind, outpatient trial comparing subjects treated with 400 mg per kilogram of IVIG every 28 days with those given 0.1% albumin placebo. CD4+ counts were measured at entry and every 12 weeks. Twenty-eight clinical centers in mainland United States and Puerto Rico participated. Previous reports showed IVIG efficacy for infection prophylaxis in 313 patients with entry CD4+ counts of > or = 0.20 x 10(9)/L (> or = 200/mm3). Two hundred and seventy-seven (89%) of these 313 children had three or more CD4+ counts measured during the trial and were included in evaluation of CD4+ count trends. Rates of CD4+ count decline, as measured by regression slopes, were compared between IVIG and placebo groups using generalized linear models, comparing unadjusted, age-adjusted, and standardized age-adjusted data. Potential covariate effects were assessed by modeling change in CD4+ count in terms of log change between successive measurements. Age-adjusted slope analysis showed slowing of CD4+ count decline by 13.5 cells/mm3 per month in IVIG compared with placebo recipients (95% confidence interval, 3.1-23.9, p = 0.012). Modeling log change between measurements documented a beneficial effect of IVIG that was cumulative over time and independent of other therapies. Occurrence of serious bacterial infection in the interval before CD4+ count measurement or death was independently associated with more rapid CD4+ count decline (p = 0.01 and p = 0.008, respectively). Zidovudine therapy was associated with a transient increase in CD4+ count. Benefits of IVIG include slowing of CD4+ count decline as well as previously reported reductions in serious and minor bacterial and viral infections in subjects with entry CD4+ counts of > or = 0.20 x 10(9)/L. This finding provides corroboration for the hypothesis that immunologic mechanisms contribute to the pathogenesis of CD4+ decline in HIV infection.
OBJECTIVES: To analyze the influence on adherence and clinical outcome of the replacement of a previous antiretroviral therapy to a simplified approach using zidovudine, lamivudine, and abacavir (Trizivir) and to assess its economic impact. METHODS: A retrospective study of 75 pretreated, HIV-infected adult patients who received Trizivir from May 2001 to December 2002. Adherence was assessed by dispensation records or medication counting, CD4 lymphocyte counts, and viral load before and six months after medication change was analyzed; finally, the cost of each therapy was assessed in order to calculate the economic impact of medication change. RESULTS: Mean adherence significantly increased a 2.5% after medication change; 16 more patients reached optimal adherence, with an NNT (number of patients requiring therapy change in order to obtain one more adherent) of 4.7. The number of patients with undetectable viral load remained almost similar, and mean CD4 cell counts stayed above 500 cells/mm3 in both periods of time. A great variability in incremental costs was seen, due to the varying costs of the previous treatments, and the influence of five intensification therapies using Trizivir. However, when only simplification regimens were analyzed such variability was reduced, and even became favorable in selected cases. CONCLUSIONS: Changing to a simplification therapy using Trizivir resulted in improved adherence, similar clinical outcomes, and a varying economic impact depending on previous antiretroviral therapy costs.
A cross sectional survey was set up to study the relation between the prevalence of allergic-type reactions during HIV infection course. For each patient, a standardized interview about recent allergic-type manifestations (RATM), skin prick-tests to six common airborne allergens, IgE serum level were done. Among the 115 included patients, the mean CD4 lymphocyte count (CD4) was 214.7/mm3 (range: 0-1328/mm3). RATM were found in 8.8% of patients with CD4 < 50, in 30% of patients with CD4 between 51 and 200, in 36% of patients with CD4 between 201 and 350 and in 11.5% of patients with CD4 < 350 (p = 0.03). The risk of presenting RATM was 4.8 times (95% confidence interval = 1.7-13.5) higher in patients with CD4 between 51 and 350 than in other patients (p = 0.003). The proportion of positive prick-tests did not significantly vary according to the level of CD4. The increased frequency of RATM in patients with CD4 between 51 and 350/mm3 could be due to an allergic predisposition acquired during the course of HIV infection. The mechanisms explaining the reduced frequency of allergic manifestations when immunodeficiency is profound (CD4 < 50/mm3) remain to be explained.
A retrospective series of 25 patients with AIDS and tuberculosis is presented. Their clinical presentation, absolute lymphocyte count, CD4+ and CD8+ lymphocyte counts, treatment details and outcome are detailed. Commonest method of acquiring HIV infection was through heterosexual contact (10 of the 25; 40%) and blood transfusion (10 of the 25; 40%). More than 50% of the patients (14 of the 25) had extrapulmonary tuberculosis. Eighteen of the 19 patients for whom values were available had CD4+ lymphocyte count < 200/mm3. Four of the 18 patients for whom follow-up details were available died.
It is now apparent that a proportion of individuals (5-8%) remains clinically free of HIV-1 disease with normal levels of CD4+ lymphocytes (> or =500/microl) for more than 8 years following infection. However, the proportion of these individuals who ultimately progress to AIDS remains to be established. We determined the virological and immunological characteristics of a cohort of long-term nonprogressors in Australia and examined the role of these factors in predicting disease progression. Individuals with documented asymptomatic HIV-1 infection for at least 8 years with CD4+ lymphocyte counts >500 cells/microl were recruited from hospital clinics and general practices serving the eastern area of Australia. CD4+ lymphocyte count, rate of CD4+ lymphocyte change, CD8+ lymphocyte count, beta2-microglobulin, immune complex dissociated (ICD) HIV-1 p24 antigen, and plasma HIV-1 RNA were measured at baseline and multiple visits at 6-month intervals over an average period of 2 years. Up to November 1996, 67 study participants were recruited, of whom 72% had been infected with HIV-1 for at least 10 years. HIV-1 RNA correlated with beta2-microglobulin, ICD p24 antigen, and the ability to isolate virus in culture but not with levels of CD4+ or CD8+ lymphocytes. Serum beta2-microglobulin was a stronger predictor of CD4+ lymphocyte decline than HIV-1 RNA and the only factor significantly associated with CD4+ lymphocyte decline. These findings show that the serum concentration of beta2-microglobulin is a strong predictor of immunological progression in people with long-term asymptomatic HIV-1 infection and provides additional prognostic information to HIV-1 RNA in determining the risk of disease progression.
Thirty patients who had hemophilia and were seropositive for the human immunodeficiency virus were evaluated. The preoperative CD4 lymphocyte count was decreased to an average of 336 x 10(9) per liter (range, 27 to 708 x 10(9) per liter). After twenty-six orthopaedic operations in patients who had no previous bacterial infection, a nosocomial infection (cellulitis in the forearm, at the site of an intravenous catheter) developed in only one patient, but five patients had an abnormal postoperative fever that was not accompanied by the expected increase in the white blood-cell count. The preoperative CD4 lymphocyte count was significantly reduced in the patients who had an abnormal elevation in body temperature (p less than 0.004). The functional result or outcome after operation was similar to that in hemophilic patients treated before 1982. Subsequent progression of infection with the human immunodeficiency virus, as determined by the CD4 lymphocyte count and the Walter Reed classification system, occurred in most patients. Acquired immunodeficiency syndrome was diagnosed in six patients. A more rapid progression to acquired immunodeficiency syndrome was seen in the patients who had a lower CD4 lymphocyte count preoperatively. Preoperative evaluation of the CD4 lymphocyte count and the response to intradermal skin-test antigens in patients who are at risk for infection postoperatively provides additional information concerning immunological competence. With these data, the possible risk of infection in patients who are seropositive for the human immunodeficiency virus can be estimated more accurately.
OBJECTIVE: This study aimed to determine if patients with HIV infection can develop a significant antibody response to influenza immunisation, and whether such immunisation is detrimental to the progression of their HIV illness. DESIGN: Prospective, non-randomised study. METHODS: The titres of antibody response to influenza immunisation were determined in 44 asymptomatic HIV positive men and compared with 16 HIV presumed seronegative controls. The magnitude of response were correlated with patients' CD4 lymphocyte counts. The rate of CD4 lymphocyte count decline over a median of 12 months before and after immunisation were also evaluated. RESULTS: Thirty-two of the 44 HIV positive subjects (73%) were able to mount a four-fold or greater response to at least one of the influenza strains, and 14 of them (32%) did so to all four strains. In comparison, 15 of the 16 controls (93.5%) had a four-fold or greater response to at least one, and six of them (38%) to all influenza strains, which was not significantly different from the HIV positive group. The magnitude of increase in antibody titre was not significantly different between the two groups either. CD4 lymphocyte count change for a median of 12 months after immunisation was not different from a median of 12 months before immunisation. CONCLUSIONS: Asymptomatic HIV infected patients are able to mount antibody response to influenza immunisation, which appears to be safe in respect to HIV illness progression in the short term.
OBJECTIVE: To assess plasma viral RNA concentration in cats naturally infected with feline immunodeficiency virus (FIV). ANIMALS: 28 FIV-infected cats. PROCEDURE: Cats were categorized into 1 of the 3 following stages on the basis of clinical signs: asymptomatic (nonclinical) carrier (AC; n = 11), acquired immunodeficiency syndrome-related complex (ARC; 9), or acquired immunodeficiency syndrome (AIDS; 8). Concentration of viral RNA in plasma (copies per ml) was determined by use of a quantitative competitive polymerase chain reaction (QC-PCR) assay. Total lymphocyte count, CD4+ cell and CD8+ cell counts, and the CD4+ cell count-to-CD8+ cell count ratio were determined by use of flow cytometry. RESULTS: Plasma viral RNA concentration was significantly higher in cats in the AIDS stage, compared with cats in AC and ARC stages. Most (5/7) cats in the AIDS stage had low total lymphocyte, CD4+ cell, and CD8+ cell counts. CONCLUSIONS AND CLINICAL RELEVANCE: Concentration of plasma viral RNA is a good indicator of disease progression in FIV-infected cats, particularly as cats progress from the ARC to the AIDS stage. Determination of CD4+ and CD8+ cell counts can be used as supportive indicators of disease progression.