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At least 487 records · Page 27Linked to original sources
PubMed2002

Study of some markers of inflammation in atherothrombotic pathogenesis of acute ischemic stroke.

Recent researches focused on the study of the role of the inflammation in the atherothrombotic pathogenesis of the acute cerebral ischemia. The aim of the study was to identify some acute phase proteins with possible role in the pathogenesis of the ischemic stroke. Some acute phase proteins were prospectively investigated by standard methods in sera of 78 patients with ischemic stroke in the first admission day. There were two groups according to neurological deficit one month after the ischemic stroke: good outcome and poor outcome. In the second group mean value of C-reactive protein (CRP) was 0.122 +/- 0.06 g/l (p < 0.01), mean value of C3 was 2.61 +/- 0.36 g/l (p < 0.01), mean value of C4 was 0.73 +/- 0.07 g/l (p < 0.05), mean value of alpha 1-antitrypsin (AAT) was 4.9 +/- 0.46 g/l (p < 0.01), mean value of alpha 1-antichymotrypsin (ACT) was 0.33 +/- 0.04 g/l (p < 0.01), mean value of alpha 1-acid glycoprotein (AGA) was 1.12 +/- 0.15 g/l, (p < 0.05), mean value of fibrinogen was 2.6 +/- 0.22 g/l (p < 0.01), mean value of haptoglobin was 2.8 +/- 0.33 g/l, (p < 0.05), mean value of transferrin was 2.8 +/- 0.26 g/l (p < 0.05), mean value of ferritin was 238 +/- 22.42 microg/l (p < 0.001), mean value of fibronectin was 2.14 +/- 0.17 g/l (p < 0.05), mean value of ceruloplasmin was 1.23 +/- 0.24 g/l (p < 0.01). High significant values of ferritine and significant values of CRP, C3, AAT, ACT and fibrinogen were observed in patients with poor outcome. The presented data suggest that the studied markers are useful to appreciate the role of the inflammatory reaction in the atherothrombotic pathogenesis of the ischemic stroke.

Acute-Phase Proteins↗
PubMed2005

[Autoimmune polyendocrine syndromes and related diseases: pathogenesis and clinical features].

Autoimmune processes are involved in the pathogenesis of diseases of several endocrine organs. There are also syndromes, where autoimmune diseases of multiple endocrine and other organs occur simultaneously. The pathogenesis of certain syndromes belonging to this group has been clarified recently and this made possible the discovery of previously unknown aspects of autoimmunity. In this review the authors present a brief synopsis of the pathogenesis and clinical features of autoimmune polyendocrine syndrome type 1 and the IPEX syndrome that are inherited as monogenic traits. Although the etiology of type 2 autoimmune polyendocrine syndrome and POEMS syndrome are not as well characterized as that of the aforementioned monogenic diseases, considering their clinical importance, the authors summarize the main features of these syndromes, as well.

Humans↗
PubMedDate not supplied

TP53 abnormalities are frequent and early events in the sequential pathogenesis of gallbladder carcinoma.

BACKGROUND: Gallbladder carcinoma (GBC) is a frequent neoplasm in Hispanic and native American populations. GBC is preceded by gallstones, chronic cholecystitis and dysplastic changes of the gallbladder epithelium. The knowledge of the molecular events involved in its pathogenesis is scarce. AIMS: We investigated the role of TP53 inactivation in the sequential pathogenesis of GBC. METHODS: Invasive tumor-, dysplastic- and histologically normal GB epithelial-cells were obtained from archival formalin-fixed tissues from GBC and GB from gallstone patients without GBC. Normal GB epithelia from 5 non-gallstone specimens were also studied. DNA extracted was examined for loss of heterozygosity (LOH) using 2 microsatellite markers and for TP53 mutations at exons 5 to 8. RESULTS: GBCs demonstrated a high frequency of LOH (81%) and mutation (67%), and both abnormalities indicating gene inactivation were detected in 52%. Similar frequency of TP53 abnormalities and gene inactivation (38%) were detected in their accompanying normal and dysplastic epithelia. Noteworthy, one third of normal and dysplastic epithelia obtained from GBs of gallstone patients without GBC demonstrated either TP53 allele loss or mutation, but gene inactivation was less frequent (11%). Most mutations affected exons 5 and 7, and they were more frequently missense point mutations. The same TP53 mutation was detected in only a subset (27%) of comparisons between non-malignant epithelia adjacent to GBCs, indicating that TP53 mutation occurs independently at several epithelial foci. CONCLUSIONS: These findings indicate that TP53 abnormalities are early and frequent events in the pathogenesis of GBC, starting from chronic cholecystitis.

Aged↗
PubMed2005

[The C46359T polymorphism of DNMT3B promoter gene and pathogenesis of acute leukemia].

OBJECTIVE: To explore the relationship between the polymorphism of C46359T in DNMT3B promoter and the pathogenesis of acute leukemia (AL). METHODS: PCR-RFLP and DNA sequencing were used to analyze the genotypic polymorphism C46359T of promoter in genomic DNA of bone marrow cells/blood lymphocytes from 160 patients with AL and 240 normal controls. RESULTS: In people of the Hans in China, genotypic frequencies of 2.5% (CT), 97.5% (TT) and 0 (CC) were statistically significant (P < 0.001) comparing with the genotype frequencies of 41.8% (CT), 23.2% (TT) and 35.0% (CC) in Caucasian in USA. The genotypic frequency of CT heterozygote in 160 AL patients was 10.6%, significantly higher than that in the control subjects (2.5%, P < 0.001), indicating that the CT heterozygote might be a more frequent phenomenon in AL. Compared with TT homozygote, CT heterozygote had a 4.669-fold increased risk of acute leukemia (OR = 4.669; 95% confidence interval 1.700-14.747). It was suggested that CT heterozygote was relative to the pathogenesis of AL. CONCLUSIONS: Different distribution of genotypes in different races, the CT heterozygote was relative to the pathogenesis of AL.

Acute Disease↗
PubMed1992

[The pathogenesis of dilated cardiomyopathy: current progress].

The pathogenesis of dilated cardiomyopathy (DCM) is still unknown; however, some factors that seem to play an important role in the development of the disease have recently been identified: they are enteroviral infections, immune mechanisms and genetic factors. Enteroviral infection (particularly due to Coxsackie virus B) has long been suspected to be the cause of myocarditis and subsequent DCM. However, only recent techniques of genetic engineering have been able to demonstrate the presence of enteroviral RNA in endomyocardial biopsy of patients with DCM. The role of the viral particles contained in the myocardium is still undetermined. Changes in the immune system concerning cell-mediated and humoral immunity have been recently detected. It has been suggested that an autoimmune process could be the actual cause of DCM in some patients, rather than the consequence. The immune system is strictly related to the major histocompatibility complex. As in some autoimmune diseases, a relationship between DCM and HLA class II phenotype has been found: particularly the DR4 antigen seems to be associated with a high risk of disease. Besides immunogenetic factors, other genetic factors seem to play a role in the pathogenesis of DCM. In 6-8% of cases a familial history of cardiomyopathy has been observed. In clinical studies on familial DCM different phenotypes have been shown, suggesting that different genetic mechanisms are involved in the pathogenesis of the disease. At least two main mechanisms can be hypothesized: the transmission of "predisposing" factors or a defect in proteins essential for the cardiac muscle cell function. Viral agents, autoimmune reactions, immunogenetic and genetic factors seem to cause myocardial damage individually or with complex interactions: the research should be devoted to these topics in the future.

Antibody Formation↗
PubMed2005

[Pathogenesis and treatment of CIDP].

CIDP is an autoimmune peripheral polyneuropathy. Clinical and electrophysiologic features indicate its heterogeneity, and such wide spectrum of the phenotype makes difficult to clarify complete pathogenesis. IVIg is an effective therapy no less than corticosteroids and plasmaphresis, and getting as the first choice for CIDP treatment due to the easy administration and less side effect. However, we have noticed that there is certain amount of non-responder, and this therapeutic heterogeneity could correspond to independent pathogenesis. In our previous report, axonal dysfunction, such as muscle atrophy and decreased CMAPs, is a significant factor to represent non-responder. Not only about therapy responsiveness, but aspect of long-term prognosis, subjects that show unfavorable prognosis indicate significant muscle atrophy and loss of myelinated fibres. Hence, decreased axonal function in peripheral nerve should critically affect CIDP pathogenesis. In practice, clinician should select proper treatment modality in light of clinical symptoms and appropriate medical costs, and if each one does not show enough efficacies, another should be admitted because responder for each modality is not necessarily overlapped. Although immunosuppressive agents might be admitted for non-responder to any other modalities, large randomized control trial is not done yet.

Humans↗
PubMedDate not supplied

Pathogenesis and pharmacologic treatment of obesity: the role of energy regulatory mechanism.

Obesity has become a worldwide public health problem affecting millions of people. This is a chronic, stigmatized, and costly disease, rarely curable and is increasing in prevalence to a point today where we define obesity as an epidemic disease that not only in developed but also on developing countries. The pathogenesis of obesity is largely unknown, especially about energy regulatory mechanism that involved wide area of neuroendocrinology that is very interesting but very complex and makes internists "refuse" to learn. Obesity occurs through a longstanding imbalance between energy intake and energy expenditure, influenced by a complex biologic system that regulates appetite and adiposity. Obesity influences the pathogenesis of hypertension, type 2 diabetes, dyslipidemia, kidney, heart, and cerebrovascular disease. It is very wise for every internist to learn the pathogenesis and treatment of this worldwide diseases. Until now, the available treatments, including drugs, are palliative and are effective only while the treatment is being actively used; and besides so many side effects reported.

Appetite Depressants↗
PubMed2005

Recent insights into the pathogenesis of severe sepsis.

OBJECTIVE: Severe sepsis remains the dominant challenge in the care of critically ill patients. Over the last 10 years a large body of research has modified our understanding of this condition. In this article, we review the evolution of our understanding of the molecular mechanisms responsible for the development of this clinical syndrome. DATA SOURCES: The authors undertook a critical review of the literature on the molecular basis of the pathogenesis of sepsis with particular emphasis on the role of cytokines, toll-like receptors, adhesion molecules, coagulation cascade molecules and the possible role of in-vitro experimental models of blood-endothelium interaction. SUMMARY OF REVIEW: Recent insights into the molecular mechanisms responsible for the pathogenesis of the severe sepsis syndrome suggest that pro- and anti- inflammatory pathways are simultaneously activated and interact in a dynamic way. Pro-inflammatory cytokines previously considered as targets for intervention have typically been already activated and de-activated by the time the clinical diagnosis is made and intervention is possible. Cellular activity involving white cell-endothelial interactions occur later, making them a more attractive option for therapeutic intervention. Immunological incompetence rather than over-activity may be the most common state of cell function in critically ill patients. CONCLUSIONS: Our understanding of the the pathogenesis of severe sepsis continues to grow. Expression of membrane surface molecules such as toll-like receptors, adhesion molecules and cytokine receptors induce a high degree of redundancy and amplification. Cell responsiveness is reduced in an attempt to circumvent the amplification loop. However, the ensuing interaction between the host and the pathogen(s) may lead to an immune deficiency, leaving the field open to further invasion by the original bacteria or to superimposed infection agents. Endothelium-white cell interactions might be an appropriate target for future interventions.

Journal Article↗
PubMedDate not supplied

Chemokines and chemokine receptors in HIV infection: role in pathogenesis and therapeutics.

Chemokines are known to function as regulatory molecules in leukocyte maturation, traffic, homing of lymphocytes and in the development of lymphoid tissues. Besides these functions in the immune system, certain chemokines and their receptors are involved in HIV pathogenesis. In order to infect a target cell, the HIV envelope glycoprotein gp120 has to interact with the cellular receptor CD-4 and co-receptor, CC or CXC chemokine receptors. Genetic findings have yielded major insights into the in vivo roles of individual co-receptors and their ligands in providing resistance to HIV infection. Mutations in chemokine receptor genes are associated with protection against HIV infections and also involved in delayed progression to AIDS in infected individuals. Blocking of chemokine receptors interrupts HIV infection in vitro and this offers new options for therapeutic strategies. Approaches have been made to study the CCR-5 inhibitors as antiviral therapies and possibly as components of a topical microbicide to prevent HIV-1 sexual transmission. Immune strategies aimed at generating anti-CCR-5 antibodies at the level of the genital mucosa might be feasible and represent a strategy to induce mucosal HIV- protective immunity. It also remains to be seen how these types of agents will act in synergy with existing HIV-1 targeted anti viral or those currently in developments. Beyond providing new perspectives in fundamental aspects of the HIV-1 transmission and pathogenesis, chemokines and their receptors suggest new areas for developing novel therapeutic and preventive strategies against HIV infections. Studies in this review were identified through a search for relevant literature in the pubmed database of the national library of medicine. In this review, some developments in chemokine research with particular focus on their roles in HIV pathogenesis, resistance and therapeutic applications have been discussed.

CCR5 Receptor Antagonists↗
PubMed2007

Hereditary hemorrhagic telangiectasia. Genetics, pathogenesis, clinical manifestation and management.

Hereditary hemorrhagic telangiectasia HHT, Morbus Osler or Osler-Weber-Rendu syndrome OMIM 187300, is an autosomal dominant disorder characterized by epistaxis, telangiectasia, multi-systemic vascular dysplasia and clinical presentation of wide variation. The pathogenesis involves dilated post-capillary venules or telangiectases in the mucus membrane of various organs as well as larger arteriovenous malformations. Genetic heterogeneity of HHT is confirmed; 2 disease loci, ACVRL1 and ENG genes, have been identified and characterized. The 2 major types of the disease, HHT1 and HHT2, are attributed to mutations in the ENG and ACVRL1 genes. ENG and ACVRL1 genes code for proteins, namely endoglin and activin-receptor-like kinase 1 ALK-1, which are members of the TGF-beta receptor family, are essential for maintaining vascular integrity. Another gene has been implicated in HHT; the HHT3 locus linked to chromosome 5. In the last 2 decades, the genetics, pathogenesis, clinical manifestations and management of HHT have been extensively researched. At this stage, it is deemed appropriate to review the wealth of information accumulated on the topic. Better understanding of the functions of endoglin, ALK-1, and other proteins involved in the pathogenesis of HHT should facilitate better management of patients with this disorder.

Humans↗
PubMed1991

Immune abnormalities in the pathogenesis of juvenile rheumatoid arthritis.

Juvenile rheumatoid arthritis (JRA) is the most common rheumatic disease of childhood. Although the etiology remains unknown, immunoregulatory imbalances are thought to be important in the pathogenesis of JRA. Numerous immunologic abnormalities have been described in these patients, but it remains unclear which are fundamental to the pathogenesis of the disease and which are secondary. In this article, the authors review lymphocyte and lymphokine abnormalities in children with JRA with emphasis on the possible role of these immune abnormalities in the pathogenesis of JRA.

Arthritis, Juvenile↗
PubMedDate not supplied

[Postmenopausal osteoporosis--definition, pathogenesis, prevention and therapy].

Osteoporosis represents one of the major health and socioeconomic problems of the modern society. Although numerous risk factors have been identified in the last decade, the pathogenesis of the disorder has not been elucidated yet. However, recent advances in the understanding of the biology of bone as well as the possibility to measure bone mass from the basis for better understanding of the of the pathogenesis of the disorder. In this review article the author discusses current hypotheses of the pathogenesis of osteoporosis with particular view to the role of estrogen deficiency, the role of calcitonin and possible involvement of other hormones and local factors. Histomorphometric studies have shown that osteroporosis is heterogenecus disorder which might explain different results obtained with different therapeutic approaches. It is well accepted that prevention of osteoporosis is more successful and therefore more important than treatment once the bone loss has occurred. In this review the author discusses primary role of estrogen replacement in the prevention of osteoporosis as well as the results of either preventive or therapeutic trials with different medications such as calcium, calcitonin, sodium fluoride and biphosphonates.

Female↗
PubMed1990

[Abnormalities of axonal transport as pathogenesis of axonal degeneration in peripheral neuropathy].

Axonal transport is a universal property of nerve cells. Role of axonal transport abnormalities in the pathogenesis of peripheral neuropathies was discussed. Applications of isotope-labeling technique to the study of axonal transport in experimental neuropathy have provided insights into the pathogenesis of axonal degeneration. As a model of dying-back neuropathy, axonal transport has been studied in sciatic motor neurons of rats with neuropathy induced by p-bromophenylacetylurea (BPAU) using this technique. The velocity of rapid anterograde transport was unaffected in this neuropathy and amount of retrograde axonal transport was reduced. The lag time between precursor injection and the onset of transport was shorter in BPAU-treated rats than controls. Whereas, in experimental ethylene oxide (EO) neuropathy rats, rapid transport velocity was markedly reduced in spite of very mild results of morphometric study. Those rapid axonal transport abnormalities may explain some aspects of the pathogenesis of peripheral neuropathies. In BPAU neuropathy model, disturbance of assembly of membrane-limited vesicles in Golgi processing may play a role in turnaround defect which causes dying-back neuropathy. EO neuropathy model suggests the possibility of oxygen utilization disturbance may causes energy dependent rapid transport velocity. Moreover, environments surrounding axon are also important for function of axonal transport. Present information leads to the conclusion that abnormalities in the supply and deposition of transported materials occur in early course of peripheral neuropathy and may contribute to development of the neuropathy.

Animals↗
PubMed1990

Studies on the pathogenesis of choriocarcinoma by analysis of restriction fragment length polymorphisms.

The association of complete hydatidiform mole with choriocarcinoma has long been recognized, but it is unknown whether the pathogenesis of the two are identical. We investigated the pathogenesis of these trophoblastic tumors by analyzing restriction fragment length polymorphisms using a minisatellite DNA probe to choriocarcinoma, the complete mole, and normal trophoblasts as well as the parental cells. The polymorphic fragments of the complete mole were all transmitted from the paternal DNA, but some polymorphic fragments of the paternal DNA were not recognized in the complete mole. This confirms at a molecular level the androgenetic origin of the complete mole. In some cases of choriocarcinoma, the pattern of inheritance of restriction fragment length polymorphisms was the same as that in the complete mole, whereas in others all the polymorphic fragments in tumor tissues were identical to those in the host DNA. These results suggest that the pathogenesis of choriocarcinoma varies, being completely different from that of the complete hydatidiform mole in some cases.

Choriocarcinoma↗
PubMed1990

Ammon's horn sclerosis: its pathogenesis and clinical significance.

Sclerosis of the cornu Ammonis or Ammon's horn sclerosis (AHS) is an "often-described, yet hitherto enigmatic phenomena" as Spielmyer put it in 1927. It has been found in cases with ischemia, anoxia or hypoglycemia and in more than half of the epileptic brains examined at autopsy. Various theories about its pathogenesis have been propounded. Among them, the "Pathoklise" theory of the Vogts and the vascular theory of Spielmeyer and his associates were prevailing until recently. In 1953, two articles were published to contribute to the pathogenesis of ictal automatism (a type of complex partial or temporal lobe seizures). One is the incisural sclerosis theory by Penfield and his associates and the other is the Ammon's horn sclerosis theory by Sano and Malamud. The former authors described a diffuse sclerosis of the infero-mesial temporal structures without, however, specifically relating it to AHS. They considered it was the result of localized anoxia of that portion of the brain caused by incisural herniation occurring during parturition. Sano and Malamud maintained that AHS is a result of convulsions, a distinct scar adjacent to which epileptogenic foci may develop in the course of time to cause ictal automatism. The latter theory was corroborated by Sano, Falconer and others. Falconer expanded the theory to the assertion that not only ictal automatism but other types of intractable epilepsy may be due to "mesial temporal (Ammon's horn) sclerosis". The most recent development in the pathogenesis of AHS is the excitotoxicity theory. Namely, AHS is caused by excessive excitation of neurons, probably by putative excitatory neurotransmitters, especially, glutamate. For this theory, there is a significant body of evidence. The problem of AHS, an old research subject and a matter of long-lasting controversy, has now been updated and become one of the newest topics in the field of experimental neurobiology.

Animals↗
PubMed1990

Pathogenesis of disease caused by Aleutian mink disease parvovirus.

A review of the pathogenesis of Aleutian mink disease parvovirus (ADV) infection based on recent knowledge gained by the author and collaborators is given. The review focuses mainly on the following topics. 1) Development of an easy, sensitive and fast assay for detection of ADV antigens and antibodies directed against these antigens. A highly sensitive rocket line immunoelectrophoretic assay (RLIE) was developed. This assay turned out to be 32 times more sensitive than the counter current electrophoresis assay routinely used to detect anti-ADV antibodies in ADV eradication programs, and moreover, ADV associated antigens could simultaneously be quantitatively detected in the same electrophoretic run. Later, the assay was improved to make it more economical and easy to use and finally the assay, now termed the counter current line absorption immunoelectrophoresis (CCLAIE) assay, was slightly modified to adapt the test to screening programs. 2) Examination of surface properties of the virus and the antigens expressed during in vivo infection. In this chapter studies on the surface charge properties of ADV are described. Using charge-shift crossed immunoelectrophoresis the occurrence of amphiphilic proteins associated with ADV is shown and the significance of these findings in regard to biological properties are discussed. The first demonstration of intact ADV structural and nonstructural proteins in mink tissues is described and it is shown that the structural proteins of the cell culture adapted strain of ADV (ADV-G) also in vivo is 2-3000 dalton smaller than those of other ADVs, i.e. 75,000 and 85,000 dalton in ADV-G as opposed to 78,000 and 88,000 dalton in the other ADVs. 3) Studies on the pathogenesis of interstitial pneumonia caused by ADV in newborn mink kits. The features of ADV-induced interstitial pneumonia are described. Using Southern blot and in situ hybridization techniques it is shown that ADV replicates to high levels in alveolar type II cells and it is suggested that the permissive replication of the virus in these cells causes direct cytopathology, followed by decreased surfactant production and development of the characteristic clinical and pathological features of respiratory distress and hyaline membrane disease. 4) Comparison of the pathogenesis of acute versus chronic disease caused by ADV infection. The data obtained by in situ hybridization analysis of ADV infected adult mink, mink kits, and mink kits treated with anti-ADV antibodies are compared. The accumulated data suggested that the development of severe acute ADV-induced disease is linked to low or absent antibody titers paired with high levels of viral replication.(ABSTRACT TRUNCATED AT 400 WORDS)

Aleutian Mink Disease↗
PubMed1990

The natural history of vasculitis. What the histology tells us about pathogenesis.

While histopathologic analysis may offer some clues as to the pathogenesis of vasculitis, observations must be interpreted with caution, as there is considerable overlap in the histologic pattern. In most cases, a predominantly neutrophilic vasculitis affecting small dermal venules suggests a relatively acute, immune complex-mediated reaction. Less commonly, this histologic pattern may be seen in non-immunologically mediated processes, such as in the presence of bacterial toxins or malignant hypertension, or in more chronic disease states, such as granuloma faciale or erythema elevatum diutinum. A predominantly lymphocytic vasculitis may represent several pathogenetic mechanisms. In lesions more than 24 to 48 hours old, a lymphocytic vasculitis may represent a resolving phase of an immune complex-mediated neutrophilic vasculitis. Alternatively, this histologic pattern may be seen de novo in conditions with a presumed cell-mediated immunologic pathogenesis. Lymphocytic vasculitis may also be seen in rickettsial infections such as Rocky Mountain spotted fever. The pathogenesis of granulomatous vasculitis remains poorly understood and is thought to be induced by a combination of circulating immune complexes and a cell-mediated immune response.

Granuloma↗
PubMed1987

Experimental transmission and pathogenesis of immunodeficiency syndrome in cats.

We describe the identification, experimental transmission, and pathogenesis of a naturally occurring powerfully immunosuppressive isolate of feline leukemia virus (designated here as FeLV-FAIDS) which induces fatal acquired immunodeficiency syndrome (AIDS) in 100% (25 of 25) of persistently viremic experimentally infected specific pathogen-free (SPF) cats after predictable survival periods ranging from less than 3 months (acute immunodeficiency syndrome) to greater than one year (chronic immunodeficiency syndrome), depending on the age of the cat at time of virus exposure. The pathogenesis of FeLV-FAIDS-induced feline immunodeficiency disease is characterized by: a prodromal period of largely asymptomatic viremia; progressive weight loss, lymphoid hyperplasia associated with viral replication in lymphoid follicles, lymphoid depletion associated with extinction of viral replication in lymphoid follicles, intractable diarrhea associated with necrosis of intestinal crypt epithelium, lymphopenia, suppressed lymphocyte blastogenesis, impaired cutaneous allograft rejection, hypogammaglobulinemia, and opportunistic infections such as bacterial respiratory disease and necrotizing stomatitis. The clinical onset of immunodeficiency syndrome correlates with the replication of a specific FeLV-FAIDS viral variant, detected principally as unintegrated viral DNA, in bone marrow, lymphoid tissues, and intestine. Two of seven cats with chronic immunodeficiency disease that survived greater than 1 year after inoculation developed lymphoma affecting the marrow, intestine, spleen, and mesenteric nodes. Experimentally induced feline immunodeficiency syndrome, therefore, is a rapid and consistent in vivo model for prospective studies of the viral genetic determinants, pathogenesis, prevention, and therapy of retrovirus-induced immunodeficiency disease.

Acquired Immunodeficiency Syndrome↗