Transient reversal of HIV-associated motor neuron disease following the introduction of highly active antiretroviral therapy.

Neurological diseases occur frequently in patients with human immunodeficiency virus (HIV) infection, and include a variety of neuromuscular disorders. On the other hand, only a few cases of motor neuron disease (MND) have been reported to date in HIV-positive patients, even though this neurological complication occurs with a 27-fold greater frequency in these subjects compared with the general population. A retroviral etiology for MND has long been hypothesized, and epidemiological and experimental data suggest a pathogenetic link between HIV infection and MND, because retroviral infections may cause motor neuron damage in both laboratory animals and humans, as a result of various pathways. Furthermore, the introduction of potent, protease inhibitor-based antiretroviral combinations has had a great impact on the natural history of HIV disease and produced a dramatic improvement in some patients with HIV-associated MND, but optimal treatment for this progressive neurological complication has not been well defined. A case of MND in a male HIV-infected patient with significant but transient reversal of neurological symptoms after the use of protease inhibitor-containing antiretroviral regimen is described.

Prevalence and virologic consequences of HIV-1 genotype mutations detected in a cohort of 161 Italian patients receiving a nelfinavir-based highly active antiretroviral therapy.

A cross-sectional study was carried out in our tertiary care hospital between January 1998 and December 2001. All 161 consecutive patients naive to nelfinavir and who had received a nelfinavir-based highly active antiretroviral therapy (HAART) of at least 24-week duration were extrapolated from the 802 adult HIV-infected subjects treated with antiretroviral therapy. All cases of virologic failure were considered and viral genotyped. Virologic failure occurred in 80 out of 161 nelfinavir-treated patients, all belonging to the experienced group. On the whole, only 11 patients (7%) developed the D30N substitution, whose 6 was in association with the N88D mutation. Among the 80 failed patients, the M184V mutation was detected in 52 (65%), while only 7 patients showed simultaneously the M184V, T215Y and K103N substitutions. In our HIV-infected population receiving a nelfinavir-based HAART, the D30N mutation has shown a low absolute frequency, while the detection of M184V substitution and the simultaneous occurrence of M184V, T215Y and K103N mutations were related to a more favorable virological response.

HIV-1, HAART and bone metabolism.

Much attention has been paid to the emerging complications of HIV infection in patients receiving HAART. Recently, there emerged a potentially increased risk of bone problems like osteopenia, osteoporosis and osteonecrosis as patients live longer. It could be a drug side effect, a consequence of prolonged exposure to HIV and/or activated immune cells characteristic of HIV infection, or a consequence of immune system changes that accompany suppression of virus by the drugs. Future research should focus on the etiologic mechanisms, define the incidence and prevalence prospectively, determine the relationship with HAART (especially the rule of protease inhibitors), and help to guide management. Only when the mechanism for HIV-related versus HAART-related changes can be defined, will we be much closer to designing specific interventions.