Die HIV-spezifische T-Zellantwort

A subset of human immunodeficiency virus type 1 long-term non-progressors is characterized by the unique presence of ancestral sequences in the viral population

“…Patients with immunological characteristics similar to our ancestral subset have been reported: Hogervorst et al (1995) described that LTNPs could be divided into two groups according to low or high p24 antibody titres. Several studies also described a subset of LTNPs with extremely low viral loads and neutralizing antibodies (Cao et al, 1995; Carotenuto et al, 1998;Harrer et al, 1996;Zhang et al, 1997). Ferbas et al (1995) identified three patients, among 12 LTNPs, with a low virus burden, but without evidence of activated circulating anti-HIV CD8 + cells.…”

“…Although HIV-infected individuals could be described by a continuous spectrum of disease-progression rates, the segregation of LTNPs into individuals with modern and ancestral viral sequences also corresponds to patients with very different virological and immunological characteristics. Based on the very low viral burden, limited viral evolution and almost normal immunological parameters, it could be inferred that the ancestral LTNPs could correspond to authentic non-progessors or at least to very slow progressors (Balotta et al, 1997;Ferbas et al, 1995;Harrer et al, 1996;Lefrère et al, 1997), whereas modern LTNP patients with a low but detectable viral burden, high viral diversity and abnormal immunological characteristics could represent the slow progressors. Therefore, ancestral viral dating in LTNPs could have prognostic value.…”

“…LTNPs have been associated with a low viral burden (Barker et al, 1998;Cao et al, 1995;Hogervorst et al, 1995;Pantaleo et al, 1995;Rinaldo et al, 1995) and a strong cellular (Barker et al, 1998;Cao et al, 1995;Harrer et al, 1996;Hogervorst et al, 1995;Klein et al, 1995;Pantaleo et al, 1995;Rinaldo et al, 1995) or humoral (Cao et al, 1995;Carotenuto et al, 1998;Hogervorst et al, 1995;Keet et al, 1994;Lifson et al, 1991;Montefiori et al, 1996;Pantaleo et al, 1995;Pilgrim et al, 1997;Zhang et al, 1997) specific immune response. Also, lower non-specific immune system activation (Buchbinder et al, 1994;Lifson et al, 1991;Sheppard et al, 1993), specific human leukocyte antigen (HLA) haplotypes (Hogan & Hammer, 2001) and supertypes (Trachtenberg et al, 2003), a 32 bp deletion in the CCR5 gene (Dean et al, 1996;Michael et al, 1997) and infection with less virulent HIV-1 strains (Cao et al, 1995;Keet et al, 1994;Learmont et al, 1992) are associated with long-term survival.…”

The Patent Situation Concerning the Treatment of Diseases Associated With Autoantibodies Directed Against G-protein-coupled Receptors

“…In parallel with the order of the detection and description of new G-protein-coupled receptor autoantibodies, the list of new patents protecting peptides or proteins of the epitope sequences for therapeutic and diagnostic purposes has been growing, as shown in Table I for the adrenergic a1-receptor [136][137][138][139][168][169][170][171], AT1-receptor [140][141][142][143][144][145][146], PAR-receptor [147][148][149][150][151], muscarinic M2-receptor [161][162][163], adrenergic b2-receptor [161][162][163][164], TSH-receptor [172][173][174][175][176][177][178][179][180][181][182][183][184][185] and endothelin-receptor autoantibodies [186][187][188][189][190]…”