SEARCH · PubMed Health

Results for “Leukoencephalopathy, Progressive Multifocal”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources

PubMedDate not supplied

The clinical spectrum of neurological manifestations in AIDS patients in Mexico.

BACKGROUND: Neurological complications may be present clinically in up to 39% of patients infected with HIV or AIDS. Some reports have shown different profiles of neurological illness related to geographic variations and the population studied. METHODS: This retrospective study describes the neurological manifestations of patients with AIDS seen between 1990 and 1998 at a single neurological referral hospital in Mexico City. RESULTS: One hundred forty-nine patients were included, 133 males (89%) and 16 females (10.7%). The average age was 33.8 years (9 to 75 years). Upon admission, only 50 patients (33.6%) were known to be seropositive to HIV-1. In 75 patients (50.3%), the neurological illness was definitory of AIDS and also was its first recognized clinical manifestation. The most common infection problems were brain toxoplasmosis (32.2%), meningeal cryptococcosis (21.5%), tuberculosis (8.7%), and AIDS-dementia complex (8.7%). There were eight (5.4%) cases of ischemic cerebrovascular disease and four (2. 7%) neoplasms. Two primary brain lymphomas and single cases of astrocytoma and oligodendroglioma, progressive multifocal leukoencephalopathy (PML), aseptic meningitis, acute encephalitis, transverse myelitis, myopathy, and cranial neuropathy were also seen. CONCLUSION: In comparison with other studies of neurological complications of AIDS, opportunistic infections amenable to treatment in our population were more common. A high case fatality rate was observed, as was a large proportion of patients in whom the neurological illness was the first manifestation of HIV infection or AIDS due to denied, unknown, or unrecognized risk factors for HIV infection.

Acquired Immunodeficiency Syndrome↗

PubMed1995

The neuropathology and epidemiology of AIDS. A Berlin experience. A review of 200 cases.

The brains of 200 patients who died with Acquired Immunodeficiency Syndrome (AIDS) from Berlin were examined retrospectively. This study was specifically intended to evaluate and document the prevalence of neuropathologic abnormalities, establishing the frequency of the various types of structural lesions, their combinations, their relative incidence, and the risk factors involved in different age groups. The data were compared and contrasted with the findings reported from other parts of the world and other German cities. It was found that the mean age of this group of patients was 41.4 years old, 75% were homosexual/bisexuals (H/B) and 18.5% were drug abusers (DA). Only 5.5% were women. Brain parenchymal changes, called in this report, HIV-related encephalopathy (HIVRE), characterized by vacuolization or spongy changes and astrocytosis in the subcortical white matter, and occasionally in gray matter, were found in 67 patients (33.5%). Drug abusers had a higher incidence of HIVRE (59.5%) compared with homosexual/bisexuals (28%). This is statistically significant (p < 0.0005). CMV encephalitis was found in 26 patients (13%) (8% of the drug abusers in contrast to 13% in the homosexual/bisexuals group). Primary central nervous system lymphoma (PCNSL) was seen in 28 patients (14%) regardless of the risk factor involved. 20 (13%) of the 150 H/B and 3 (8%) of the 37 DA had CMV encephalitis. Of the 150 H/B, 24 (16%) had PCNSL compared with only 4 of 37 (11%) of the DA. A significant incidence of opportunistic infections, both protozoal and viral was found in all groups. Cerebral toxoplasmosis occurred in 68 patients (34%). Microglial (phagocytic) nodules, probably related to CMV or cerebral Toxoplasmosis, were observed in 40 cases (20%). Diffuse microglial proliferation was noted in 104 patients (52%). Cerebral cryptococcosis was found in three patients. Progressive multifocal leukoencephalopathy was seen in 16 patients (8%). Various combinations of CNS pathological processes were found in 44 of the patients (22%). These include concomitant infections with Toxoplasma gondii and HIVRE in 13 patients; Toxoplasmosis and PCNSL in 8 patients; Toxoplasmosis with CMV and HIVRE in 4 patients; Toxoplasmosis with CMV in 2 patients; Toxoplasmosis with PCNSL and CMV in 2 patients; Toxoplasmosis with PCNSL and HIVRE in 2 patients and Toxoplasmosis with PML and HIVRE in 2 patients; Cerebral CMV with PCNSL and HIVRE in 4 patients; Cerebral CMV with HIVRE in 2 patients; PML with PCNSL in one patient; PML with HIVRE in 2 patients; and PML with PCNSL and HIVRE in one patient. Cerebrovascular lesions were found in 34 patients (17%).(ABSTRACT TRUNCATED AT 400 WORDS)

AIDS Dementia Complex↗

PubMed2000

Human polyomavirus JC variants in Papua New Guinea and Guam reflect ancient population settlement and viral evolution.

The peopling of the Pacific was a complex sequence of events that is best reconstructed by reconciling insights from various disciplines. Here we analyze the human polyomavirus JC (JCV) in Highlanders of Papua New Guinea (PNG), in Austronesian-speaking Tolai people on the island of New Britain, and in nearby non-Austronesian-speaking Baining people. We also characterize JCV from the Chamorro of Guam, a Micronesian population. All JCV strains from PNG and Guam fall within the broad Asian group previously defined in the VP1 gene as Type 2 or Type 7, but the PNG strains were distinct from both genotypes. Among the Chamorro JCV samples, 8 strains (Guam-1) were like the Type 7 strains found in Southeast Asia, while nine strains (Guam-2) were distinct from both the mainland strains and most PNG strains. We identified three JCV variants within Papua New Guinea (PNG-1, PNG-2 and PNG-3), but none of the Southeast Asian (Type 7) strains. PNG-1 strains were present in all three populations (Highlanders and the Baining and Tolai of New Britain), but PNG-2 strains were restricted to the Highlanders. Their relative lack of DNA sequence variation suggests that they arose comparatively recently. The single PNG-3 strain, identified in an Austronesian-speaking Tolai individual, was closely related to the Chamorro variants (Guam-2), consistent with a common Austronesian ancestor. In PNG-2 variants a complex regulatory region mutation inserts a duplication into a nearby deletion, a change reminiscent of those seen in the brains of progressive multifocal leukoencephalopathy patients. This is the first instance of a complex JCV rearrangement circulating in a human population.

Adult↗

PubMed2005

Drug insight: using monoclonal antibodies to treat multiple sclerosis.

Multiple sclerosis (MS) is an immunopathological, presumably autoimmune, disease of the CNS. Several immunomodulatory treatments, including various preparations of interferon-beta, glatiramer acetate and mitoxantrone, have been approved for MS therapy. Because these agents are only partially effective, the search for better therapies continues. Therapeutic monoclonal antibodies (mAbs), a class of biotechnological agents, allow the precise targeting of molecules involved in pathological processes. Therapeutic mAbs have shown much promise in the treatment of many disorders, including inflammatory and putative autoimmune diseases such as MS. These agents have intrinsic limitations, however, such as induction of neutralizing 'anti-antibodies', systemic inflammatory reactions and severe adverse effects, some of which remain to be explained. Most notably, natalizumab (Tysabri), a mAb against alpha4 integrin, was very effective in suppressing MS activity, but had to be withdrawn from the market because several treated patients developed progressive multifocal leukoencephalopathy. This article reviews the state of development of various therapeutic mAbs for MS treatment.

Animals↗

PubMed2005

Blocking adhesion molecules as therapy for multiple sclerosis: natalizumab.

Immunologists have long hypothesized that particular 'molecular addresses' govern lymphocyte entry to a given organ. In 1992, alpha4beta1 integrin was identified as the key molecule involved in homing to inflamed regions of the brain. An antibody to alpha4beta1integrin blocked paralysis in an animal model of multiple sclerosis, and the humanized monoclonal antibody natalizumab, which binds alpha4beta1 integrin, reduced relapses 66% in clinical trials in multiple sclerosis. Three months after its expedited approval by the FDA, natalizumab was removed from the market after two cases of deadly progressive multifocal leukoencephalopathy were reported among the few thousand patients who had taken this drug in those clinical trials.

Animals↗

PubMed2005

Finding new tricks for old drugs: an efficient route for public-sector drug discovery.

With the annotation of the human genome approaching completion, public-sector researchers - spurred in part by various National Institutes of Health Roadmap Initiatives - have become increasingly engaged in drug discovery and development efforts. Although large and diverse chemical libraries of 'drug-like' compounds can be readily screened to yield chemically novel scaffolds, transforming these 'chemical probes' into drugs is a daunting endeavour. A more efficient approach involves screening libraries of approved and off-patent medications; both phenotypic- and molecular target-based screening of 'old drugs' can readily yield compounds that could be immediately used in clinical trials. Using case studies, we describe how this approach has rapidly identified candidate medications suitable for clinical trials in disorders such as progressive multifocal leukoencephalopathy and amyotrophic lateral sclerosis. This approach has also led to the discovery of the molecular targets responsible for serious drug side effects, thereby allowing efficient 'counter-screening' to avoid these side effects.

Anti-Bacterial Agents↗

PubMed1999

Human ubiquitous JCV(CY) T-antigen gene induces brain tumors in experimental animals.

JCV is a papovavirus which is widespread in the human population. The prototype Mad-1 variant of JCV induces a fatal demyelinating disease of the central nervous system (CNS) called Progressive Multifocal Leukoencephalopathy (PML) in immunosuppressed individuals. The unique tropism of JCV (Mad-1) to the CNS is attributed to the tissue-specific regulation of the viral early promoter which is responsible for the production of the viral regulatory protein, T-antigen. The archetype form of this virus, JCV(CY), which has been repeatedly isolated from the urine of PML and non-PML individuals, is distinct from JCV(Mad-1) in the structural organization of the regulatory sequence. To characterize the tissue specific expression of JCV(CY) and to investigate its potential in inducing disease, transgenic mice containing the early region of JCV(CY) were generated. Some of these mice between 9-13 months of age exhibited signs of illness as manifested by paralysis of rear limbs, hunched posture, and poor grooming. Neuropathological examination indicated no sign of hypomyelination of the brain, but surprisingly, revealed the presence of primitive tumors originating from the cerebellum and the surrounding brain stem. The tumor masses also infiltrated the surrounding tissue. Results from RNA and protein studies revealed a high level of T-antigen mRNA expression in hindbrains of clinically normal and affected transgenic mice. However, higher levels of T-antigen RNA and protein were detected in brains of the animals exhibiting severe illness. The close resemblance of JCV(CY) induced tumor in transgenic mice to the human medulloblastoma/primitive neuroectodermal tumor (PNETs) in location, histologic appearance, and expression of marker proteins strongly suggests the utility of this novel animal model for the study of human brain tumors.

Animals↗

PubMed2004

JCV T-antigen interacts with the neurofibromatosis type 2 gene product in a transgenic mouse model of malignant peripheral nerve sheath tumors.

The human polyomavirus, JC virus, has recently been associated with several human CNS tumors, including medulloblastomas and a broad range of glial-origin tumors. This ubiquitous virus is the causative agent of the rare demyelinating disease, progressive multifocal leukoencephalopathy in immunocompromised individuals. Expression of the viral protein, T-antigen, which possesses the ability to transform cells of neural origin, has been detected in human CNS tumors. In an effort to further understand the transforming potential of JCV T-antigen, transgenic mice expressing JCV T-antigen under the control of the Mad-4 promoter were generated. As described previously, approximately 50% of the animals developed pituitary tumors by 1 year of age. However, a small subset of the animals developed solid masses arising from the soft tissues surrounding the salivary gland, the sciatic nerve, and along the extremities that histologically resemble malignant peripheral nerve sheath tumors, rare neoplasms that occur in individuals with neurofibromatosis type 1 (NF1). JCV T-antigen was detected in tumor tissue by immunohistochemistry and immunoprecipitation/Western blotting, but not in normal tissues and was colocalized with NF2, the putative tumor suppressor protein associated with neurofibromatosis type 2, in the nucleus of some cells. In addition, T-antigen was co-precipitated with NF2, but not with NF1 protein, although NF1 was detectable in tumor tissue. Furthermore, precipitated immunocomplexes contained T-antigen, NF2, and p53, suggesting that these three proteins may form a ternary complex. The importance of these findings on mechanisms of T-antigen-mediated tumorigenesis and the pathogenesis of neurofibromatosis are discussed. Oncogene (2004) 23, 5459-5467. doi:10.1038/sj.onc.1207728 Published online 10 May 2004

Animals↗

PubMed2003

Viral regulatory region sequence variations in kidney tissue obtained from patients with BK virus nephropathy.

BACKGROUND: The polyomavirus genome contains a noncoding control region (NCCR), which is believed to contain the enhancer elements that are important activators of viral transcription. We hypothesized that DNA sequence variations in this region play a role in the pathogenesis of BK virus allograft nephropathy (BKVAN). METHODS: Tissue sections were prepared from 26 paraffin-embedded biopsies with BKVAN obtained from 15 patients. The sections were lysed in a proteinase K buffer and subjected to DNA sequencing using Big Dye cycle sequencing reactions run on an automated DNA sequencer (ABI 310). NCCR anatomy was compared to the genomic sequence of archetype BKV strain WW. RESULTS: Twelve putative transcription factor binding sites showed nucleotide substitutions, deletions, or duplications in at least one of the biopsies studied. Changes were most commonly found in binding sites for granulocyte/macrophage stimulating factor promoter (24/26 biopsies) and nuclear factor-I (NF-I) transcription factor (21/22 biopsies). Less frequent changes were seen at other binding sites, including T antigen (3/22 biopsies) and the cytomegalovirus immediate early (CMV IE-1) promoter (3/22 biopsies). Five biopsies showed complex rearrangements reminiscent of those described in JC virus-associated progressive multifocal leukoencephalopathy. CONCLUSION: The regulatory region of BKV shows sequence heterogeneity in biopsy tissue with viral nephropathy. Sequence variations frequently affect putative transcription factor binding sites, with potential implications for promoter activity related to genes important in viral replication. Architectural rearrangements were found in some cases but did not appear to be a prerequisite for the pathogenesis of BKVAN.

BK Virus↗

PubMed1998

Diagnosing HIV-related disease: using the CD4 count as a guide.

OBJECTIVE: To summarize current information on the relation between CD4 counts and the risk of different HIV-related diseases. MEASUREMENTS AND MAIN RESULTS: MEDLINE search of English language articles between 1985 and 1996 using the medical subject heading (MeSH) term "CD4 lymphocyte count" and searches using key words of multiple HIV-related diseases were conducted. Some HIV-related diseases can be stratified to different CD4 count levels. Regardless of their CD4 count, HIV-infected patients are susceptible to sinusitis, Kaposi's sarcoma, community-acquired pneumonia, and oral hairy leukoplakia. In advanced HIV, when CD4 is below 200/mm3, Pneumocystis carinii pneumonia, toxoplasmosis, progressive multifocal leukoencephalopathy, Mycobacterium avium complex, molluscum contagiosum, and bacillary angiomatosis all increase in incidence. In very advanced HIV disease, when CD4 counts are below 50/mm3, patients are at risk of pseudomonas pneumonia, cytomegalovirus retinitis, central nervous system lymphoma, aspergillosis, and disseminated histoplasmosis.

AIDS-Related Opportunistic Infections↗

PubMed2001

Neurolymphomatosis associated with muscle and cerebral involvement caused by natural killer cell lymphoma: a case report and review of literature.

We report a biopsy-proven case of neurolymphomatosis (NL) presenting with sensory motor axonal polyneuropathy, polymyositis, and cerebral involvement. Ours is the second reported case of NL caused by natural killer-cell lymphoma defined by morphology and immunophenotyping. For 3 months, the patient developed stocking-glove distribution of hypesthesia, subacute progressive weakness and mental deterioration. EMG showed severe sensorimotor mixed axonal-demyelinating polyradiculoneuropathy. Lumbar puncture revealed mildly high protein level with normal glucose and cell count. Sural nerve biopsy demonstrated lymphomatous axonal neuropathy and muscle biopsy was indicative of lymphomatous polymyositis. Brain MRI revealed multiple white matter lesions, consistent either with progressive multifocal leukoencephalopathy or cerebral lymphoma. Bone marrow biopsy showed neoplastic infiltrates. The patient died of multiple organ failure prior to initiation of chemotherapy.

Bone Marrow↗

PubMed2002

BK virus regulatory region rearrangements in brain and cerebrospinal fluid from a leukemia patient with tubulointerstitial nephritis and meningoencephalitis.

BK virus (BKV) was recovered by polymerase chain reaction (PCR) from brain, kidney, lung, urine, and cerebrospinal fluid (CSF) of a fatal case of BKV tubulointerstitial nephritis with dissemination to lung and brain. Viral regulatory regions in PCR-amplified urine and the lung samples were identical to the archetypal structure, WWT. In the brain and CSF, a rearranged sequence predominated, however. A 94-bp deletion preceded a 71-bp tandem duplication because the same 94-bp segment was deleted from both copies. PCR-amplified regulatory region products were cloned and sequenced to define further the extent of the rearranged structures. Two kidney clones were archetypal, whereas two others were rearranged differently from the brain and from each other. In contrast to the brain clones, the kidney rearrangements seemed to involve deletion after duplication. Three of four brain clones sequenced were identical to the rearrangement found to dominate in the PCR product. A fourth clone showed two short deletions without any duplication. The four CSF clones all showed rearrangements identical to that which was amplified by PCR from CSF and brain. This represents the first molecular analysis of a BKV strain obtained from a central nervous system infection, and it reveals regulatory region rearrangements reminiscent of those described in JC virus from brains with progressive multifocal leukoencephalopathy. We suggest that the presence in the CSF of BKV with a dominant rearranged regulatory region may be useful in the diagnosis of BKV meningoencephalitis secondary to BKV nephritis.

BK Virus↗

PubMed1999

Opportunistic viral infections in the setting of human immunodeficiency virus.

Human immunodeficiency virus (HIV) infection has provided a setting in which additional neurologic problems develop. The mechanism of these complications varies from agent to agent, but the added spectrum of diseases encountered has challenged diagnosticians and provided unparalleled opportunities to develop a deeper understanding of these conditions and their treatments. This review addresses the most prominent viral-associated complications, except for progressive multifocal leukoencephalopathy, which is addressed in a separate review. The complications of greatest importance both due to their frequency and severity are caused by cytomegalovirus, so these are discussed in greater depth. However, the association of Epstein-Barr virus with induction of central nervous system lymphoma represents an important viral linked complication of great importance. In addition, the increased activity of varicella zoster virus has been notable in the setting of HIV. Finally, human herpesvirus type 6 is an emerging virus of interest that has been identified in the setting of HIV infection, whose role in pathophysiology is only now being investigated.

AIDS-Related Opportunistic Infections↗

PubMed1987

Regulation of the host range of human papovavirus JCV.

Human papovavirus JCV is associated with the human demyelinating disorder progressive multifocal leukoencephalopathy. In tissue culture, the virus is largely restricted to growth in primary human fetal glial cell. In this study, we demonstrate two levels of regulation of the viral host range. Expression of the early JCV mRNA, which encodes the essential viral protein, large tumor antigen (T antigen), depends on recognition of the early enhancer/promoter elements by tissue-specific factors found in both human and rodent glial cells. In the presence of JCV T antigen, viral DNA replication requires a species-specific factor, presumably a component of DNA polymerase, which is found in a wide range of primate cells. We further demonstrate that simian virus 40 T antigen has sufficient homology to efficiently substitute for the analogous JCV protein in initiating viral DNA replication.

Animals↗

PubMed1990

Trans-activation of the JC virus late promoter by the tat protein of type 1 human immunodeficiency virus in glial cells.

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of the central nervous system caused by the JC virus (JCV), a human papovavirus. PML is a relatively rare disease seen predominantly in immunocompromised individuals and is a frequent complication observed in AIDS patients. The significantly higher incidence of PML in AIDS patients than in other immunosuppressive disorders has suggested that the presence of human immunodeficiency virus type 1 (HIV-1) in the brain may directly or indirectly contribute to the pathogenesis of this disease. In the present study we have examined the expression of the JCV genome in both glial and non-glial cells in the presence of HIV-1 regulatory proteins. We find that the HIV-1-encoded trans-regulatory protein tat increases the basal activity of the JCV late promoter, JCVL, in glial cells. In a reciprocal experiment, the JCV early protein, the large tumor antigen, stimulates expression from JCVL and HIV-1 long terminal repeat promoter in both glial and non-glial cells. This trans-activation occurs at the level of RNA synthesis, as measured by the rate of transcription, stability of the message, and translation. We conclude that the presence of the HIV-1-encoded tat protein may positively affect the JCV lytic cycle in glial cells by stimulating JCV gene expression. Our results suggest a mechanism for the relatively high incidence of PML in AIDS patients than in other immunosuppressive disorders. Furthermore, our findings indicate that the HIV-1 regulatory protein tat may stimulate other viral and perhaps cellular promoters, in addition to its own.

Cell Line↗

PubMed1994

The POU domain protein Tst-1 and papovaviral large tumor antigen function synergistically to stimulate glia-specific gene expression of JC virus.

Synergism between transcriptional activators is a powerful way of potentiating their function. Here we show that the glial POU domain protein Tst-1 (also known as Oct-6 and SCIP) and large tumor antigen (T antigen) synergistically increased transcription from both the early and the late promoters of papovavirus JC in glial cells. Synergism between both proteins did not require T-antigen-mediated DNA replication or direct binding of T antigen to the promoter. The ability of T antigen to functionally cooperate with Tst-1 was contained within its N-terminal region, shown by the fact that small tumor antigen (t antigen) could substitute for T antigen in transfection experiments. In addition to this functional synergism, a direct interaction between Tst-1 and T antigen was observed in vitro. Using deletion mutants of Tst-1 and T antigen, the POU domain of Tst-1 and the N-terminal region of T antigen were found to participate in this interaction. Because of the low levels of Tst-1 present in oligodendrocytes, synergism between Tst-1 and T antigen could be an important factor in establishing the lytic infection of oligodendrocytes by JC virus during the course of the fatal demyelinating disease progressive multifocal leukoencephalopathy.

Antigens, Polyomavirus Transforming↗

PubMed1996

Detection of JC virus DNA sequence and expression of the viral oncoprotein, tumor antigen, in brain of immunocompetent patient with oligoastrocytoma.

We describe molecular and clinical findings in an immunocompetent patient with an oligoastrocytoma and the concomitant presence of the human papovavirus, JC virus (JCV), which is the etiologic agent of the subacute, debilitating demyelinating disease, progressive multifocal leukoencephalopathy. Histologic review revealed a glial neoplasm consisting primarily of a moderately cellular oligodendroglioma with distinct areas of a fibrillary astrocytoma. Immunohistochemical analysis revealed nuclear staining of tumor cells with antibodies against the viral oncoprotein [tumor antigen (T antigen)], the proliferation marker (Ki67), and the cellular proliferation regulator (p53). Using primers specific to the JCV control region, PCR yielded amplified DNA that was identical to the control region of the Mad-4 strain of the virus. PCR analysis demonstrated the presence of the genome for the viral oncoprotein, T antigen, and results from primer extension studies revealed synthesis of the viral early RNA for T antigen in the tumor tissues. The presence of viral T antigen in the tumor tissue was further demonstrated by immunoblot assay. To our knowledge, this is the first report of the presence of JCV DNA, RNA, and T antigen in tissue in which viral T antigen is localized to tumor cell nuclei and suggests the possible association of JCV with some glial neoplasms.

Antigens, Neoplasm↗

PubMed1997

Typing of urinary JC virus DNA offers a novel means of tracing human migrations.

Although polyomavirus JC (JCV) is the proven pathogen of progressive multifocal leukoencephalopathy, the fatal demyelinating disease, this virus is ubiquitous as a usually harmless symbiote among human beings. JCV propagates in the adult kidney and excretes its progeny in urine, from which JCV DNA can readily be recovered. The main mode of transmission of JCV is from parents to children through long cohabitation. In this study, we collected a substantial number of urine samples from native inhabitants of 34 countries in Europe, Africa, and Asia. A 610-bp segment of JCV DNA was amplified from each urine sample, and its DNA sequence was determined. A worldwide phylogenetic tree subsequently constructed revealed the presence of nine subtypes including minor ones. Five subtypes (EU, Af2, B1, SC, and CY) occupied rather large territories that overlapped with each other at their boundaries. The entire Europe, northern Africa, and western Asia were the domain of EU, whereas the domain of Af2 included nearly all of Africa and southwestern Asia all the way to the northeastern edge of India. Partially overlapping domains in Asia were occupied by subtypes B1, SC, and CY. Of particular interest was the recovery of JCV subtypes in a pocket or pockets that were separated by great geographic distances from the main domains of those subtypes. Certain of these pockets can readily be explained by recent migrations of human populations carrying these subtypes. Overall, it appears that JCV genotyping promises to reveal previously unknown human migration routes: ancient as well as recent.

Adult↗