Damage to secondary lymphoid follicles in AIDS-related persistent generalized lymphadenopathy, as revealed by the behaviour of dendritic reticulum cells possessing immunoreactive acid cysteine-proteinase inhibitor

Alavaikko, M; Rinne, Ari; Järvinen, Mikko; Vk, Hopsu-Havu; Aine, Risto; Levine, A. Joan; Pr, Meyer; Lukes, RJ

doi:10.1007/bf02889909

Cited by 10 publications

(4 citation statements)

References 16 publications

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“…15 Reduced Cystatin A expression has been found in secondary lymphoid follicles in lymph node material from individuals with AIDS-related persistent generalized lymphadenopathy (PGL). 16 This finding seems to correspond to the morphologic changes in the FDC network used by Biberfeld et al 17 for staging of HIV-1 infection in lymphoid tissue, and thus suggests a relation between expression of Cystatin A and fragmentation of the FDC network in HIV-1 infection. In a preliminary study, we have presented a quantitative method for measuring fragmentation of lymphoid follicles (fragmentation rate [FR]) during HIV-1 infection and have shown that fragmentation is reversed by highly active antiretroviral therapy (HAART).…”

supporting

confidence: 65%

Cystatin A and HIV-1 p24 Antigen Expression in Tonsillar Lymphoid Follicles During HIV-1 Infection and During Highly Active Antiretroviral Therapy

Voltersvik¹,

Bostad²,

Dyrhol-Riise³

et al. 2006

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Cystatin A is a natural cysteine proteinase inhibitor and is found in a wide variety of normal cells. The physiologic role of Cystatin A is not fully known, however. Cystatin A is present in large amounts in follicular dendritic cells, which are important in HIV-1 pathogenesis. We analyzed Cystatin A expression in tonsillar sections from 20 patients at various stages of HIV-1 infection. There was a significant (P < 0.001) difference in Cystatin A fractions between patients and controls, with medians (ranges) of 0.61 (0.46-0.83) and 0.86 (0.78-0.90), respectively. Inverse correlations (Spearman rho) existed between Cystatin A and the rate of follicular fragmentation (rho = -0.658) and HIV-1 p24 antigen expression (rho = -0.622) in germinal centers and the amount of HIV-1 RNA in tonsillar tissue (rho = -0.765). The Cystatin A fraction declined from early chronic HIV-1 infection and was significantly lower in patients with a CD4 count below as compared with above 300 cells/muL of blood (P < 0.001), suggesting a favorable initiation of highly active antiretroviral therapy (HAART) at this level. Regeneration of Cystatin A to normal levels was shown in 11 patients 12 and 48 weeks after initiation of HAART, whereas the rate of follicular fragmentation was still elevated. Thus, we found Cystatin A to be a sensitive marker during HIV-1 infection and for regeneration of follicular lymphoid tissue during HAART.

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supporting

confidence: 65%

Cystatin A and HIV-1 p24 Antigen Expression in Tonsillar Lymphoid Follicles During HIV-1 Infection and During Highly Active Antiretroviral Therapy

Voltersvik¹,

Bostad²,

Dyrhol-Riise³

et al. 2006

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…Later, some pathologists noted the presence of FL in HIV-free pa tients [1,[11][12][13]. Guettier et al [12] clearly showed the existence of FL, i.e.…”

Section: Discussionmentioning

confidence: 99%

“…FL was initially regarded as a specific change in HIV-infected nodes [8][9][10]. Later, however, a few articles reported the presence of FL in HIV-free nodes [11][12][13][14]. As analysis of HIV-free FL has been quite limited and different authors use the term FL in different ways, it is still not certain if the FL in HIV-free nodes is in fact identical to that of HIV-infected nodes.…”

Section: Introductionmentioning

confidence: 99%

Follicle Lysis in HIV-Free Lymphoid Tissues

Shiota

Toyama²,

Mori³

1990

Int Arch Allergy Immunol

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Follicle lysis (FL), the ‘moth-eaten’ degeneration of follicular dendritic cells (FDCs), previously regarded as specific for HIV-infected lymph follicles, was later claimed to exist in HIV-free patients. This study was performed to clarify the differences between HIV-free and HIV-induced FL. HIV-free and HIV-infected lymphoid tissues were analyzed immunohistologically. Most of HIV-free FLs were shown to lack the dark zones, the areas in germinal center composed mostly of much larger and clumped noncleaved cells, whereas HIV-induced FL in persistent generalized lymphadenopathy (PGL) lymph nodes included highly proliferative dark zones. Thus, FL in HIV-free lymphoid organs was suggested to be a physiological degenerative process with poor proliferative activity, while FL in PGL nodes includes two processes, FDC degeneration and B lymphocyte proliferation.

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“…During the 1980s, researchers studying secondary lymphoid tissues from infected individuals observed large amounts ofthe human immunodeficiency virus (HIV) trapped on the dendritic processes of follicular dendritic cells (FDC) (1)(2)(3)(4)(5)(6)(7). Virus trapping results in persistent generalized lymphadenopathy, eventual destruction of FDC and lysis of the lymphoid follicles (5,(8)(9)(10)(11). At the same time FDC are destroyed, viral RNA in germinal centers decreases and there is a concomitant increase in circulating levels of infectious virions (12).…”

Section: Introductionmentioning

confidence: 99%

Follicular dendritic cells (FDC) in retroviral infection: host/pathogen perspectives

Burton

Masuda

Heath

et al. 1997

Immunological Reviews

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Follicular dendritic cells (FDC) are found in the follicles of virtually all secondary lymphoid tissues. In health, these cells trap and retain antigens (Ag) in the form of immune complexes and preserve them for months in their native conformation. FDC thus serve as a long-term repository of extracellular Ag important for induction and maintenance of memory responses. In retroviral infection, FDC trap and retain large numbers of retroviral particles with profound effects on FDC. FDC-trapped retrovirus induces follicular hyperplasia, and conventional Ag trapped prior to infection are lost and new Ag cannot be trapped. Concomitantly, antibody-forming cells (AFC) specific for Ag lost from FDC decrease followed by loss of specific serum antibody (Ab). Eventually, FDC die and follicular lysis occurs. From the pathogen perspective, binding to FDC is remarkably beneficial, bringing together virus and activated target cells that are highly susceptible to infection. Furthermore, FDC permit HIV to infect surrounding cells even in the presence of a vast excess of neutralizing Ab. Preliminary data suggest that FDC maintain virus infectivity-even when the virus cannot replicate. Thus retrovirus infection monopolizes FDC networks, thereby transforming the FDC Ag repository into a highly infectious retroviral reservoir.

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Damage to secondary lymphoid follicles in AIDS-related persistent generalized lymphadenopathy, as revealed by the behaviour of dendritic reticulum cells possessing immunoreactive acid cysteine-proteinase inhibitor

Cited by 10 publications

References 16 publications

Cystatin A and HIV-1 p24 Antigen Expression in Tonsillar Lymphoid Follicles During HIV-1 Infection and During Highly Active Antiretroviral Therapy

Cystatin A and HIV-1 p24 Antigen Expression in Tonsillar Lymphoid Follicles During HIV-1 Infection and During Highly Active Antiretroviral Therapy

Follicle Lysis in HIV-Free Lymphoid Tissues

Follicular dendritic cells (FDC) in retroviral infection: host/pathogen perspectives

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