[Hemodialysis Increases the Incidence of Post-Traumatic Seizure in Hemodialysis Patients with Traumatic Intracranial Hemorrhage].

BACKGROUND: In Japan, the number of hemodialysis patients increases every year, along with the average age of this patient population. Further, certain complications of hemodialysis make the care of traumatic head injury(THI)patients particularly difficult. OBJECTIVE: This study was aimed at investigating the occurrence of and risk factors for post-traumatic seizures in hemodialysis patients with a history of THI, and determining patient outcomes. METHODS: Subjects were selected from patients who were admitted to Yaizu Municipal Hospital in Shizuoka, Japan for traumatic intracranial hemorrhage(TICH). Retrospective medical histories of TICH patients who were and were not receiving hemodialysis were reviewed to investigate the risk factors for seizures and to determine patient outcomes. RESULTS: We identified 18 THI patients on hemodialysis and 86 THI patients not on hemodialysis treatment. We determined that predictive factors of post-traumatic seizure include:current hemodialysis treatment, enlargement of an existing hematoma, and an acute subdural hematoma. Moreover, 66.7% of seizures in our dialysis patients occurred during hemodialysis. Our data also suggest that Glasgow Coma Scale(GCS)scores on admission are a predictive factor for patient outcomes following discharge. CONCLUSION: Current hemodialysis treatment, enlargement of an existing hematoma, and an acute subdural hematoma are predictive factors of seizure occurrence in THI patients. As post-traumatic seizures triggered unfavorable outcomes in some dialysis patients, it is important to create appropriate plans for preventing dialysis disequilibrium syndrome that may lead to seizures in TICH/TIH patients on hemodialysis. We also determined that a low GCS score upon admission is a significant predictor of unfavorable outcomes.

Seminal plasma and semen amyloids enhance cytomegalovirus infection in cell culture.

Among the modes of transmission available to the cytomegalovirus (CMV) is sexual transmission, primarily via semen. Both male-to-female (M-F) and male-to-male (M-M) sexual transmission significantly contribute toward the spread of CMV infections in the global population. Semen plays an important role in carrying the viral particle that invades the vaginal or rectal mucosa, thereby initiating viral replication. Both semen and seminal plasma (SP) can enhance HIV-1 infection in cell culture, and two amyloid fibrils, semen-derived enhancer of viral infection (SEVI) and amyloids derived from the semenogelins (SEM amyloids), have been identified as seminal factors sufficient to enhance HIV-1 infection (J. Munch et al., Cell 131:1059-1071, 2007; N. R. Roan et al., Cell Host Microbe 10:541-550, 2011; F. Arnold et al., J. Virol. 86:1244-1249, 2012). Whether SP, SEVI, or SEM amyloids can enhance other viral infections has not been extensively examined. In this study, we found that SP, SEVI, and SEM amyloids strongly enhance both human CMV (HCMV) and murine CMV infection in cell culture. SEVI and SEM amyloids increased infection rates by >10-fold, as determined by both flow cytometry and fluorescence microscopy. Viral replication was increased by 50- to 100-fold. Moreover, viral growth curve assays showed that SP, SEVI, and SEM amyloids sped up the kinetics of CMV replication such that the virus reached its replicative peak more quickly. Finally, we discovered that SEM amyloids and SEVI counteracted the effect of anti-gH in protecting against CMV infection. Collectively, the data suggest that semen enhances CMV infection through interactions between semen amyloid fibrils and viral particles, and these interactions may prevent HCMV from being neutralized by anti-gH antibody.

Demographics, clinical characteristics, IFNL3- and IFNL4- polymorphisms in a cohort of hepatitis C patients from Puerto Rico.

OBJECTIVE: To describe the risk factors for infection, complications, treatment received and response in Puerto Ricans with HCV attending gastroenterology clinics at UPR-MSC, and the prevalence of single nucleotide polymorphisms (SNPs) in IFNL3 and IFNL4 in this population. METHODS: After consent, demographic and medical data were obtained and blood samples were drawn from each patient. The QIAamp Blood-Maxi Kit was employed for DNA extraction. The TaqMan allelic discrimination assay was employed for SNP genotyping. HCV-RNA was measured by branched-chain DNA assay. Frequency distributions were used to describe the study population and the prevalence of SNPs. The UPR Medical Sciences Campus IRB approved the study. RESULTS: Of 259 patients recruited, 64% were men. Genotype 1was found in 112/136 (82%). Of 150 subjects treated, 19% had sustained virological response (SVR), 40% received treatment with pegylated interferon plus ribavirin. The SNP frequencies (n = 239) of IFNL3 locus rs12979860 were 27% (C/C), 50% (C/T), and 23% (T/T), and for rs8099917 were 46% (T/T), 47% (T/G), and 7% (G/G). SNP frequencies of IFNL4 locus ss469415590 were 26% (TT/TT), 48% (TT/ΔG), and 26% (ΔG/ΔG). CONCLUSION: HCV-infected Hispanics in our sample (all of which were Puerto Rican) were shown to have a low SVR rate of 19%. The demographic characteristics were similar to those of other study groups in the US, except for the annual income. Genotype-1 was the most prevalent in those patients with known HCV genotypes. This study group showed significant differences with frequencies observed in other populations. Lower frequencies of the favorable genotypes were found in our group compared with the populations having European and Asian ancestry.

Characterization of human endogenous retroviral elements in the blood of HIV-1-infected individuals.

We previously reported finding the RNA of a type K human endogenous retrovirus, HERV-K (HML-2), at high titers in the plasma of HIV-1-infected and cancer patients (R. Contreras-Galindo et al., J. Virol. 82:9329-9236, 2008.). The extent to which the HERV-K (HML-2) proviruses become activated and the nature of their activated viral RNAs remain important questions. Therefore, we amplified and sequenced the full-length RNA of the env gene of the type 1 and 2 HERV-K (HML-2) viruses collected from the plasma of seven HIV-1-infected patients over a period of 1 to 3 years and from five breast cancer patients in order to reconstruct the genetic evolution of these viruses. HERV-K (HML-2) RNA was found in plasma fractions of HIV-1 patients at a density of ∼1.16 g/ml that contained both immature and correctly processed HERV-K (HML-2) proteins and virus-like particles that were recognized by anti-HERV-K (HML-2) antibodies. RNA sequences from novel HERV-K (HML-2) proviruses were discovered, including K111, which is specifically active during HIV-1 infection. Viral RNA arose from complete proviruses and proviruses devoid of a 5' long terminal repeat, suggesting that the expression of HERV-K (HML-2) RNA in these patients may involve sense and antisense transcription. In HIV-1-infected individuals, the HERV-K (HML-2) viral RNA showed evidence of frequent recombination, accumulation of synonymous rather than nonsynonymous mutations, and conserved N-glycosylation sites, suggesting that some of the HERV-K (HML-2) viral RNAs have undergone reverse transcription and are under purifying selection. In contrast, HERV-K (HML-2) RNA sequences found in the blood of breast cancer patients showed no evidence of recombination and exhibited only sporadic viral mutations. This study suggests that HERV-K (HML-2) is active in HIV-1-infected patients, and the resulting RNA message reveals previously undiscovered HERV-K (HML-2) genomic sequences.

A one month high fat diet disrupts the gut microbiome and integrity of the colon inducing adiposity and behavioral despair in male Sprague Dawley rats.

High-fat diet (HFD) is associated with gut microbiome dysfunction and mental disorders. However, the time-dependence as to when this occurs is unclear. We hypothesized that a short-term HFD causes colonic tissue integrity changes resulting in behavioral changes. Rats were fed HFD or low-fat diet (LFD) for a month and gut microbiome, colon, and behavior were evaluated. Behavioral despair was found in the HFD group. Although obesity was absent, the HFD group showed increased percent weight gain, epididymal fat tissue, and leptin expression. Moreover, the HFD group had increased colonic damage, decreased expression of the tight junction proteins, and higher lipopolysaccharides (LPS) in serum. Metagenomic analysis revealed that the HFD group had more Bacteroides and less S24-7 which correlated with the decreased claudin-5. Finally, HFD group showed an increase of microglia percent area, increased astrocytic projections, and decreased phospho-mTOR. In conclusion, HFD consumption in a short period is still sufficient to disrupt gut integrity resulting in LPS infiltration, alterations in the brain, and behavioral despair even in the absence of obesity.

Roles of polypyrimidine tract binding proteins in major immediate-early gene expression and viral replication of human cytomegalovirus.

Human cytomegalovirus (HCMV), a member of the beta subgroup of the family Herpesviridae, causes serious health problems worldwide. HCMV gene expression in host cells is a well-defined sequential process: immediate-early (IE) gene expression, early-gene expression, DNA replication, and late-gene expression. The most abundant IE gene, major IE (MIE) gene pre-mRNA, needs to be spliced before being exported to the cytoplasm for translation. In this study, the regulation of MIE gene splicing was investigated; in so doing, we found that polypyrimidine tract binding proteins (PTBs) strongly repressed MIE gene production in cotransfection assays. In addition, we discovered that the repressive effects of PTB could be rescued by splicing factor U2AF. Taken together, the results suggest that PTBs inhibit MIE gene splicing by competing with U2AF65 for binding to the polypyrimidine tract in pre-mRNA. In intron deletion mutation assays and RNA detection experiments (reverse transcription [RT]-PCR and real-time RT-PCR), we further observed that PTBs target all the introns of the MIE gene, especially intron 2, and affect gene splicing, which was reflected in the variation in the ratio of pre-mRNA to mRNA. Using transfection assays, we demonstrated that PTB knockdown cells induce a higher degree of MIE gene splicing/expression. Consistently, HCMV can produce more viral proteins and viral particles in PTB knockdown cells after infection. We conclude that PTB inhibits HCMV replication by interfering with MIE gene splicing through competition with U2AF for binding to the polypyrimidine tract in MIE gene introns.

The long journey to the discovery of PARK2: The 50th Anniversary of Japanese Society of Neuropathology.

Research into familial Parkinson's disease (PD) remained at a virtual standstill in Europe and the US for several decades until a re-challenge by Japanese neurologists regarding an autosomal recessive form of PD. In 1965, our research group at Nagoya University examined familial cases of early-onset parkinsonism characterized by autosomal recessive inheritance, diurnal fluctuation of symptoms (alleviation after sleep), foot dystonia, good response to medication, and benign course without dementia. An inborn error of metabolism in some dopamine-related pathway was suspected. The clinical study of four families with the disease, named as "early-onset parkinsonism with diurnal fluctuation (EPDF)", was published in Neurology in 1973. The pathological study of a case in 1993 revealed neuronal loss without Lewy bodies in the substantia nigra. Based on these clinical and pathological evidences, EPDF was defined as a distinct disease entity. Screening for the EPDF gene was started in 1994 in collaboration with Juntendo University. With the discovery of parkin gene in 1998, EPDF was designated as PARK2. Of our 16 families examined for gene analysis, 15 proved to be PARK2, and the remaining one, PARK6.

Inflammatory Biomarkers, Microbiome, Depression, and Executive Dysfunction in Alcohol Users.

Alcohol-related disorders (ARD) are highly prevalent among Latin American-Caribbean countries. Mental disorders are common comorbidities in individuals with ARD. However, the etiology of the association between ARD and mental disorders remains unclear. We examined the association of inflammatory cytokines, microbiome, and other biomakers with measures of depression, social anxiety, and executive functions. We observed a significant increase in cytokine and chemokine expression levels in saliva and plasma in the alcohol group (AG) samples. Also, the salivary bacterial composition in the AG revealed an abundance of Prevotella. Depression symptomatology was markedly higher in the AG, but social anxiety levels were negligible. AG also exhibited executive dysfunctions, which negatively correlated with increased plasma levels of pro-inflammatory cytokines and increased salivary concentrations of Prevotella bacteria. Our study suggests that chronic alcohol use correlates with executive dysfunction, immune system dysregulation, and dysbiosis of the salivary microbiota. Additional studies are needed to understand the role of the microbiome and inflammation in alcohol use and mental comorbidities.

Identification and characterization of a novel germline p53 mutation in a patient with glioblastoma and colon cancer.

Germline mutations in the p53 tumor suppressor gene have been identified in patients with Li-Fraumeni syndrome (LFS) and patients with Li-Fraumeni-like syndrome (LFL). However, to date, germline p53 mutations in patients not fulfilling the criteria of LFS or LFL have been reported only very rarely. In our study, a novel germline c.584T>C (p.Ile195Thr) mutation of the p53 gene was found in a 21-year-old male with a glioblastoma and colon cancer. He had no family history of cancer within second-degree relatives, and loss of the wild-type p53 allele and overexpression of p53 protein were observed in both tumors. Functional analyses revealed transactivation and growth suppressive function activities of the Thr195-type p53 to be impaired. These results suggest germline p53 mutations to possibly be responsible for a subset of young adult patient with multiple malignant tumors, even those not meeting the clinical criteria for LFS or LFL.

GC-MS confirmation of xylazine (Rompun), a veterinary sedative, in exchanged needles.

In order to assess the extent of xylazine (Xyz) injection in Puerto Rico, two waves of used-syringe collections were performed. In the first, syringes were gathered, anonymously and without additional information; in the second, a short interview, also anonymous, was administered. We found Xyz in 37.6% of the collected syringes; the majority of the Xyz-containing syringes came from ranching communities. Syringes containing Xyz more frequently also contained "speedball" than those without (90.6% and 66.7%, respectively). Self-reports of Xyz injection deviated markedly from actual detection: only 50% (self-described users) and 22% (self-described non-users) of the collected syringes contained the drug. With a high prevalence of skin ulcers (38.5% vs. 6.8%; p<0.001), Xyz users were more likely to be in poor health compared to non-users. Surprisingly, though a higher percentage of Xyz users than non-users had college-level educations (23.1% vs. 5.5%), they were more likely to be homeless (64.1% vs. 37%).

P-glycoprotein expression in HTLV-III cells after treatment with HIV-1 protease inhibitors.

INTRODUCTION: P-glycoprotein (P-gp), a membrane protein that pumps drugs out of cells, affects the availability and effectiveness of drugs and their extrusion from cells. HIV-1 protease inhibitors (PIs), part of the antiretroviral treatment known as highly active antiretroviral treatment, are substrates and possibly inhibitors of the P-gp pump. Their interaction may represent a potential effect on treatment efficiency. Our objective is to evaluate how the P-gp/PI interaction limits drug effectiveness. METHODS: HTLV IIIcc cell cultures were exposed to ritonavir and saquinavir for 24 hours. Supernatant solution was recovered for viral load assessment. Cells were labeled with monoclonal antibody against P-gp and analyzed by flow cytometery. RESULTS: Upregulation in P-gp expression from 1% to 7% was observed when cells were exposed to PIs, compared with cells not exposed to PIs (P = .05). Ritonavir 10 microg/mL caused a similar P-gp increment as did 20 microg/ mL saquinavir. To evaluate P-gp functionality, cells were exposed to rhodamine-123, a fluorescent dye that is also a P-gp substrate. Its accumulation was measured by flow cytometry. Slightly more rhodamine was observed in cells treated with higher PI concentration (P = .05). Higher viral load was obtained in suspension of cells with upregulated P-gp. Statistically significant decreased viral load was obtained in supernatants of cells expressing less P-gp (P < .04). Ritonavir 20 microg/mL caused the most marked reduction in viral load. CONCLUSIONS: Our results suggest that the use of PIs upregulates the expression of P-glycoprotein on HTLV IIIcc cells, showing slightly inhibited functionality for those treated with higher concentrations. The rapid extrusion of the drug by P-gp seems to limit its action. Decreased viral load in suspensions with ritonavir 20 microg/mL may represent the inactivation of the transport pump, allowing the drug to work more efficiently.

A new procedure for the quantitative assessment of p-glycoprotein efflux pump associated with human T lymphocytes.

INTRODUCTION: P-glycoprotein (P-gp), a multidrug transporter located in plasma membranes, reduces intracellular availability of some drugs. Upregulation of P-gp has been observed in some clinical situations, including chronic inflammatory disease and viral infection. However, P-gp is expressed in only a small subset of peripheral blood mononuclear cells (PBMC) and at much lower quantities than it is on P-gp-positive cell lines used in other studies. METHODS: P-gp expression was assessed by flow cytometry by using a commercially available, anti-P-gp, allophycocyanin-conjugated monoclonal antibody. Flow cytometry was also used to determine the efflux activity associated with P-gp; with this process, refluxed fluorescent P-gp substrate, rhodamine 123 (Rho123), was determined by the subsequently identified P-gp-positive PBMC subset. Use of verapamil during the dye-loading procedure maximized the amount of dye retained by the cells. RESULTS: The use of allophycocyanin-conjugated monoclonal antibody allowed for the identification of P-gp-positive PBMC subsets, even when the cells were fully loaded with Rho123. We used a logical gating strategy to identify a P-gp-positive PBMC subset, after which P-gp efflux activity of the PBMC subset could be quantitatively assessed. This new procedure enabled us to assess the P-gp efflux function of T lymphocytes in some clinical situations, which induced P-gp upregulation in vivo. CONCLUSION: This new procedure enables us to quantitatively assess the P-gp efflux activity associated with PBMC.

Sanger and Next Generation Sequencing Approaches to Evaluate HIV-1 Virus in Blood Compartments.

The implementation of antiretroviral treatment combined with the monitoring of drug resistance mutations improves the quality of life of HIV-1 positive patients. The drug resistance mutation patterns and viral genotypes are currently analyzed by DNA sequencing of the virus in the plasma of patients. However, the virus compartmentalizes, and different T cell subsets may harbor distinct viral subsets. In this study, we compared the patterns of HIV distribution in cell-free (blood plasma) and cell-associated viruses (peripheral blood mononuclear cells, PBMCs) derived from ART-treated patients by using Sanger sequencing- and Next-Generation sequencing-based HIV assay. CD4⁺CD45RA-RO⁺ memory T-cells were isolated from PBMCs using a BD FACSAria instrument. HIV pol (protease and reverse transcriptase) was RT-PCR or PCR amplified from the plasma and the T-cell subset, respectively. Sequences were obtained using Sanger sequencing and Next-Generation Sequencing (NGS). Sanger sequences were aligned and edited using RECall software (beta v3.03). The Stanford HIV database was used to evaluate drug resistance mutations. Illumina MiSeq platform and HyDRA Web were used to generate and analyze NGS data, respectively. Our results show a high correlation between Sanger sequencing and NGS results. However, some major and minor drug resistance mutations were only observed by NGS, albeit at different frequencies. Analysis of low-frequency drugs resistance mutations and virus distribution in the blood compartments may provide information to allow a more sustainable response to therapy and better disease management.

Cigarette Smoking Modulation of Saliva Microbial Composition and Cytokine Levels.

Tobacco use has been implicated as an immunomodulator in the oral cavity and contributes to the development of oral cancer. In the present study, we investigated the effects of cigarette smoking on bacterial diversity and host responses compared to healthy nonsmoking controls. Saliva samples were collected from eighteen smokers and sixteen nonsmoking individuals by passive drool. The 16S rRNA gene was used to characterize the salivary microbiome by using the Illumina MiSeq platform. Cytokine and chemokine expression analyses were performed to evaluate the host response. Significant differences in cytokine and chemokine expression levels of MDC, IL-10, IL-5, IL-2, IL-4, IL-7, adrenocorticotropic hormone (ACTH), insulin, and leptin were observed between smokers and nonsmokers. Taxonomic analyses revealed differences between the two groups, and some bacterial genera associated with the smokers group had correlations with hormones and cytokines identified as statistically different between smokers and nonsmokers. These factors have been associated with inflammation and carcinogenesis in the oral cavity. The data obtained may aid in the identification of the interactions between the salivary microbiome, host inflammatory responses, and metabolism in smokers.

Molecular Epidemiology of HIV-1 Virus in Puerto Rico: Novel Cases of HIV-1 Subtype C, D, and CRF-24BG.

HIV-1 subtype B virus is the most prevalent subtype in Puerto Rico (PR), accounting for about 90% of infection in the island. Recently, other subtypes and circulating recombinant forms (CRFs), including F(12_BF), A (01_BF), and CRF-39 BF-like, have been identified. The purpose of this study is to assess the distribution of drug resistance mutations and subtypes in PR. A total of 846 nucleotide sequences from the period comprising 2013 through 2017 were obtained from our "HIV Genotyping" test file. Phylogenetic and molecular epidemiology analyses were performed to evaluate the evolutionary dynamics and prevalence of drug resistance mutations. According to our results, we detected a decrease in the prevalence of protease inhibitor, nucleoside reverse transcriptase inhibitor (NRTI), and non-NRTI (NNRTI) resistance mutations over time. In addition, we also detected recombinant forms and, for the first time, identified subtypes C, D, and CRF-24BG in PR. Recent studies suggest that non-subtypes B are associated with a high risk of treatment failure and disease progression. The constant monitoring of viral evolution and drug resistance mutation dynamics is important to establish appropriate efforts for controlling viral expansion.

HIV-1 infection increases the expression of human endogenous retroviruses type K (HERV-K) in vitro.

Antibodies to HERV-K antigens have been linked to HIV-1 infection and expression of HERV-K proteins generates T-cell cytotoxic responses in many cancers. HERV-K RNA and protein abundance was measured in HIV-1-infected and control cells. In vitro exposure of HIV-1 laboratory-adapted and primary isolates on U87MG cells increased the expression of HERV-K RNA in a dose-dependent manner. HERV-K RNA and protein burdens were significantly increased in HIV-1-producing H9 cell lines compared to H9 cells. The expression of HERV-K was synergistically increased in HIV-1-infected PBMCs after stimulation with PMA/ionomycin. Furthermore, the expression of HERV-K in PBMCs, and particularly in CD4(+) T cells, was higher in HIV-1 patients compared to control subjects. The expression of HERV-K might be related to HIV-1 pathogenesis and AIDS-associated cancers.

Comparative longitudinal studies of HERV-K and HIV-1 RNA titers in HIV-1-infected patients receiving successful versus unsuccessful highly active antiretroviral therapy.

The viral kinetics of HERV-K in HIV-1-infected patients receiving highly active antiretroviral therapy (HAART) is not unknown. HERV-K kinetic modeling may provide insight into factors altering the effectiveness of HAART in suppressing HIV-1 burden. We conducted a longitudinal study measuring the HERV-K RNA titers in four patients with successful HIV-1-suppressive HAART and in six patients undergoing HAART failure. HERV-K titers were usually undetectable in patients with successful HAART, and when detected, HERV-K titers remained below 5000 copies/ml. On the other hand, HERV-K RNA was consistently detected in patients who failed to respond to HAART before and after HIV-1 rebounds (p < 0.001). Elevated HERV-K RNA titers frequently preceded HIV-1 rebounds. These results suggest that HERV-K viral load may predict HIV-1 reactivation. HERV-K RNA testing might be clinically useful in predicting the onset of HIV-1 resistance due to suboptimal antiretroviral drug levels and/or poor adherence to treatment.

[The long journey to the discovery of PARK2].

It was acknowledged long ago that Parkinson's disease (PD) occur rarely in familial aggregations. Willige and Mjönes noted no difference between the clinical features of the familial form and those of sporadic PD. Research into this aspect remained at a standstill for several decades thereafter. The resurgence of research into familial parkinsonism was the discovery by Japanese neurologists of autosomal recessive form of PD. In 1965, at Nagoya University, our research group examined familial cases of early onset parkinsonism. Clinical features included autosomal recessive inheritance, symptomatic alleviation after sleep, hyperreflexia, foot dystonia, good response to medication, and benign course without dementia. The clinical study of four families of the disease (EPDF) was published in Neurology in 1973. Subsequently, I kept on with my study of EPDF at Hiroshima University. Pathological study by our group in 1993 revealed neuronal loss in the substantia nigra without Lewy bodies. Based on these clinical and pathological evidences, EPDF was successfully defined as a distinct disease entity. Screening for the EPDF gene was started in 1994 in collaboration with Juntendo University. With the discovery of parkin gene in 1998, EPDF was designated as PARK2. Of our 16 families examined for gene analysis, fifteen proved to be PARK2, and the resting one, PARK6.

"Pure" Suprasellar Schwannoma Presented with Communicating Hydrocephalus: A Case Report.

Schwannoma is a benign peripheral nerve sheath tumor originating from Schwann cells. Most intracranial schwannomas arise from vestibular nerve and schwannoma in the suprasellar region is extremely rare. A 64-year-old man presented with walking disturbance and blurred vision for three months. Lateral hemianopsia in the left eye and brachybasia were observed. Magnetic resonance imaging revealed a suprasellar tumor with strong contrast enhancement associated with communicating hydrocephalus. The cerebrospinal fluid tap test improved gait disturbance. Hypothalamic stimulation test revealed hypo-reaction of GH, FSH and LH. After ventriculo-peritoneal shunting, the tumor was totally removed via a bilateral front-basal approach with a clinical diagnosis of craniopharyngioma. No adhesion was observed between the tumor and surrounding structures such as meninges and brain. The histopathological diagnosis was schwannoma. Here we report a case of suprasellar schwannoma associated with communicating hydrocephalus that has not ever been previously reported, with special reference to its pathogenesis.

Detection of HERV-K(HML-2) viral RNA in plasma of HIV type 1-infected individuals.

Approximately 8% of the human genome sequence is composed by human endogenous retroviruses (HERVs), most of which are defective. HERV-K(HML-2) is the youngest and most active family and has maintained some proviruses with intact open reading frames (ORFs) that code for viral proteins that may assemble into viral particles. Many HERV-K(HML-2) sequences are polymorphic in humans (present in some individuals but not in others) and probably many others may be unfixed (not inserted permanently in a specific chromosomal location of the human genome). In the present study HIV-1 and HCV-1-positive plasma samples were screened for the presence of HERV-K(HML-2) RNA in an RT-PCR using HERV-K pol specific primers. HERV-K(HML-2) viral RNA sequences were found almost universally in HIV-1(+) plasma samples (95.33%) but were rarely detected in HCV-1 patients (5.2%) or control subjects (7.69%). Other HERV-K(HML-2) viral segments of the RNA genome including gag, prt, and both env regions, surface (su), and transmembrane (tm) were amplified from HERV-K pol-positive plasma of HIV-1 patients. Type 1 and type 2 HERV-K(HML- 2) viral RNA genomes were found to coexist in the same plasma of HIV-1 patients. These results suggest the HERV-K(HML-2) viral particles are induced in HIV-1-infected individuals.