Search

This is an audit of a new technique to improve the colposcopy service. Samples were tested for high risk HPV DNA using Digene Hybrid Capture II. Sixty-four percent of the sampled women under 30 had detectable high risk HPV DNA, decreasing to 44% in 30–39 year olds and to 27% in women over 40. High risk HPV prevalence increased with severity of cytology, although 22% with normal colposcopy had detectable high risk HPV. Of those women treated for cervical dysplasia, 83% had detectable high risk HPV prior to treatment, compared to only 32% afterwards. The audit has shown that high risk HPV testing has considerable discriminatory value. It has been integrated successfully into the service, particularly to manage low grade cervical abnormalities and to add valuable information following treatment for cervical dysplasia. Results need to be interpreted alongside colposcopy, cytology, and histology, and care must be taken in the interpretation of a single high risk HPV result. J. Med. Virol. 76:576–582, 2005. © 2005 Wiley-Liss, Inc.

We report clinical, radiological and virological data from nine consecutive HIV-infected patients with herpes simplex virus (HSV) infection of the central nervous system (CNS). Three patients presented with confusion, two with fever and headache, two with anxiety and depression, one with slow mentation and memory loss and one with expressive dysphasia. Five patients had previous AIDS-defining diagnoses: four of these five patients had previous cutaneous HSV infection. HSV DNA was detected by the polymerase chain reaction (PCR) on cerebrospinal fluid (CSF) in seven patients. HSV infection was diagnosed by brain biopsy (after negative PCR on CSF) in one patient and at autopsy in one patient (after negative CSF PCR and brain biopsy). Seven patients received specific anti-viral therapy; two died of unrelated causes and the other five recovered. Two patients were not treated, in one the diagnosis was made at autopsy and the other recovered spontaneously. HIV-infected patients with CNS HSV infection have a varied presentation. Diagnosis by PCR on CSF identified the majority of cases. With specific treatment the outcome was good.

Pre-emptive treatment strategies based on sensitive screening for cytomegalovirus (CMV) infection up to day +100 after allogeneic transplantation have been shown to reduce the incidence of CMV disease during the period of surveillance. However, the use of ganciclovir has been associated with delays in immune reconstitution and an increased incidence of late CMV disease after day +100. In the present study, 81 patients undergoing allogeneic transplantation received polymerase chain reaction (PCR)-guided pre-emptive therapy based on detection of CMV DNA by PCR on 2 consecutive weeks up to day +180. Thirty-three of the 52 high-risk patients (CMV-seropositive donor or recipient) received a total of 45 treatment episodes up to day +100. Three of these patients (5.7%) developed CMV disease, with one fatality. Twelve of the surviving 44 high-risk patients (27%) required pre-emptive treatment between days +101 and +192, but none of these patients developed late CMV disease with a median follow-up of 402 d (range 117-952 d). Antiviral therapy was stopped after a single negative PCR result with no subsequent episodes of CMV disease while patients remained off antiviral treatment. As all initial episodes of CMV DNA detection occurred within 60 d of transplantation, it may be possible to discontinue monitoring beyond day +100 in patients who have remained CMV PCR negative before this. Thus, we have confirmed that PCR-guided pre-emptive therapy results in a low incidence of CMV disease before day +100 and that discontinuing treatment on the basis of viral clearance as determined by CMV PCR appears to be safe practice. In addition, we have observed no episodes of late CMV disease with an extension of surveillance to 26 weeks.

The detection of viral genome (that is, viral nucleic acid, either DNA or RNA) has gained enormous importance over the last decade in the diagnosis and management of viral infections and diseases (table 1). Nucleic acid testing (NAT) has proven its superiority over more conventional laboratory techniques in several areas, for example: View this table: Table 1 Detection of viral genome (qualitative): clinical applications As well as qualitative analysis, the characterisation of viruses by analysis of the amplified region of the genome allows the detection and identification of viral types or subtypes and mutants. This is now used to monitor patients on highly active antiretroviral therapy (HAART), based on the multitude of resistance associated mutations that have been characterised in HIV infected patients receiving antiretroviral treatment.1 This allows a more rational therapeutic approach. Sequence analysis has also proved to be a valuable epidemiological tool—for example, to investigate possible links between cases of infection, as in outbreaks of hepatitis B2 and hepatitis C infection.3 In addition to qualitative analysis and genome sequencing, methods have been developed for the quantification of viral genomes. While initially largely applied in the research field, quantitative NAT has recently been introduced into routine diagnostic virology. In this review, we will briefly introduce the different methods available for viral genome quantification, define their place in clinical virology, and speculate on the possible future role of quantitative genomic testing for viral infections. In principle, molecular biological assays that …

OBJECTIVES: To compare the results of magnetic resonance imaging (MRI) and thallium-201 (201Tl) SPET scanning with laboratory analyses including CSF DNA detection, brain biopsy, and necropsy in the discrimination of cerebral lymphoma and toxoplasmosis in patients with AIDS. METHODS: A retrospective study of 32 patients infected with HIV who had focal CNS lesions on MRI as a result of either lymphoma or toxoplasmosis. RESULTS: 18 patients had lymphoma, 12 had toxoplasmosis, and two had both. Toxoplasma IgG antibodies were detected in only seven patients--four with toxoplasmosis, two with lymphoma, and one with both diagnoses. Epstein-Barr virus DNA was detected in CSF of all six patients with lymphoma and none of two with toxoplasmosis. MRI showed multiple lesions in 23 patients, appearances did not discriminate between lymphoma and toxoplasmosis; nine patients had single lesions, of these eight had lymphoma (p = 0.044, two tailed Fisher's exact test) 201Tl SPET showed accumulation in 17 with lymphoma and six with toxoplasmosis (p = 0.034, two tailed Fisher's exact test). Of nine patients with single lesions on MRI and 201Tl SPET with focal accumulation eight had lymphoma. 201Tl SPET uptake ratios of > or = 2.9 were only seen with lymphoma. CONCLUSION: Knowledge of patients' toxoplasma serostatus does not aid discrimination between lymphoma and toxoplasmosis. Single lesions on MRI with focal accumulation of 201Tl strongly suggest lymphoma. Multiple lesions on MRI with 201Tl SPET uptake ratios > or = 2.9 also suggest lymphoma; uptake ratios less than 2.1 do not aid discrimination. Detection of Epstein-Barr virus DNA in CSF is highly sensitive and specific for cerebral lymphoma.

OBJECTIVES—To determine the frequency and clinical relevance of Epstein-Barr virus (EBV) and Kaposi's sarcoma associated herpesvirus (KSHV) DNA detection in the CSF from patients infected with HIV. METHODS—Cerebrospinal fluid was obtained prospectively from 115 consecutive patients infected with HIV undergoing diagnostic lumbar puncture for investigation of neurological disease. Amplification of DNA was performed using a nested polymerase chain reaction (PCR) for detection of EBV internal repeat and KSHV minor capsid sequences. RESULTS—EBV DNA was detected in the CSF supernatant of 18 patients. This included all patients with primary CNS lymphoma (seven patients) or a combination of systemic and CNS lymphoma (two patients). By contrast EBV DNA was not detected in the CSF supernatant of any patient with systemic, but not CNS, lymphoma (10 patients). EBV DNA was also detected in the supernatant of nine further patients without a diagnosis of lymphoma at the time of lumbar puncture, two of whom subsequently developed CNS lymphoma. No EBV DNA was detected in CSF supernatant from the remaining 87 samples (two of these patients subsequently developed lymphoma). KSHV DNA was detected in the CSF of two patients, one had systemic (but not CNS) lymphoma and the other did not have lymphoma. CONCLUSION—A diagnosis of CNS lymphoma is strongly associated with the presence of EBV DNA in CSF. In the absence of clinical and radiological features of CNS lymphoma, the presence of detectable CSF EBV DNA may predict subsequent tumour development. KSHV DNA is rarely detected in CSF in this patient group and shows no correlation with lymphoma or other neurological disease.

The aim of this prospective study was to determine the frequency and clinical significance of detection of varicella-zoster virus (VZV) DNA in cerebrospinal fluid (CSF) from 120 HIV-infected individuals. Six of 8 CSF samples from patients with recent (up to 8 months previously) or concurrent cutaneous zoster contained detectable VZV DNA using the polymerase chain reaction. No detectable CSF VZV DNA was present in two patients who had an encephalopathy complicating cutaneous zoster or in 112 other patients without a history of recent of concurrent zoster. In conclusion, VZV DNA may be detected in CSF of patients with neurological disease and concurrent or recent zoster. However, the absence of detectable VZV DNA in CSF does not preclude the possibility of VZV associated neurological complications.

OBJECTIVES: To describe the presenting features, clinical and laboratory diagnosis, response to treatment, and outcome of necrotising herpetic retinopathy (NHR) in HIV infected patients. METHODS: Retrospective case records/laboratory data review of five HIV infected patients presenting to the specialist HIV/AIDS unit at UCL Hospitals, London from April 1994 to August 1996 with a clinical diagnosis of NHR. RESULTS: All patients had advanced HIV disease with a median CD4 count of 20.10(6)/1. Three patients had cutaneous varicella zoster virus (VZV) infection within the preceding 8 weeks. All had uniocular loss of visual acuity; one also had headache and another ocular pain. All had typical retinal appearances. VZV DNA was detected in cerebrospinal fluid of four patients (and in vitreous fluid of one of the four) and in vitreous fluid of one other. One patient refused therapy and rapidly became blind. Four patients received intravenous foscarnet with intravenous aciclovir for 6 weeks: three subsequently received oral famciclovir and one oral valaciclovir; two patients also had intravitreal injections of foscarnet. In none of the four did treatment bring about improvement in visual acuity, but in all four visual loss from retinitis was halted. CONCLUSIONS: NHR occurs in HIV infected patients with advanced HIV disease and is strongly associated with evidence of VZV infection. With aggressive use of antiviral drugs the outcome is not uniformly poor.

OBJECTIVES: To compare the results of clinical assessment and MRI with neuropathological findings in the diagnosis of HIV and cytomegalovirus (CMV) associated CNS disease. METHODS: A retrospective study of 35 patients infected with HIV who were examined at necropsy between four and 70 (median 20) days after neurological assessment and MRI. RESULTS: Of the 35 patients, 19 had diffuse white matter hyperintensity on T2 weighted MRI, six of whom also had focal lesions. Nine other patients had focal white matter lesions and seven had changes in cortical atrophy only. Necropsy in the 19 with diffuse white matter hyperintensity showed HIV leukoencephalopathy (HIVLEP) with encephalitis in 10, CMV encephalitis in three, both HIVLEP/HIV encephalitis and CMV encephalitis in one, lymphoma in three, and non-specific inflammation in two. Necropsy in the 16 other patients without diffuse white matter hyperintensity showed CMV encephalitis in six, HIV encephalitis (without HIVLEP) in two, CMV encephalitis and HIVLEP/HIV encephalitis in one, non-HIV associated abnormalities in five, herpes simplex encephalitis in one, and lymphoma in one. CMV DNA was detected in CSF of five of seven patients with CMV encephalitis and in two of two with CMV associated polyradiculopathy but without CMV encephalitis. Diffuse white matter hyperintensity on MRI had a sensitivity of 100%, a specificity of 66.6%, and a positive predictive value of 58% for diagnosis of HIVLEP. CONCLUSION: Diffuse white matter hyperintensity on MRI can be due to either HIV or CMV associated pathology or non-specific abnormalities.

OBJECTIVES: To describe the abnormalities in CSF from HIV infected patients with acute lumbosacral polyradiculopathy (ALP) caused by cytomegalovirus (CMV) infection. METHODS: Retrospective case notes and laboratory records were reviewed for 17 consecutive patients with CMV associated ALP admitted to specialist HIV/AIDS units at UCL Hospitals and Chelsea and Westminster Hospital. RESULTS: Infection with CMV was confirmed by detection of CMV DNA by polymerase chain reaction amplification in 15 patients (all of whom were negative by culture), by culture in one patient, and by objective clinical response to anti-CMV treatment in one patient. Only nine patients had a CSF pleocytosis 28-1142 (median 150) cells/mm3; in seven there was a polymorphonuclear (PMN) leucocyte preponderance. Protein concentrations in CSF were moderately or considerably raised in 13 patients; CSF: plasma glucose ratios were < or = 50% in five patients. Two patients had no pleocytosis, normal CSF: plasma glucose, and normal or near normal protein values. CONCLUSIONS: Abnormalities in CSF in CMV associated ALP are varied: only 50% of patients have a "typical" PMN preponderant pleocytosis. The diagnosis of this condition should not rely on demonstration of a PMN preponderant pleocytosis, but on identification of CMV DNA in CSF and the exclusion of other opportunistic infections and lymphoma in order that specific anti-CMV treatment may be instituted.

Introduction Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease of persons with an impaired cell-mediated immune response. Although previously rare and affecting predominantly those with lymphoproliferative disorders,* the advent of the AIDS epidemic has resulted in a dramatic increase in the incidence of PML 2 Approximately 4% of patients with AIDS develop PML and in half of them it is the initial AIDS defining illness. 3 Progressive multifocal leukoencephalopathy was first described by Anstrom et aL in 1958. 4 The association of this disorder with a viral infection was initially demonstrated by ZuRhein and Chou 5 and, independently, by Silverman and Rubenstein. 6 Both pairs of authors reported the presence of papovirus-like particles in oligodendrocytic nuclei in brain tissue.S' 6 Further confirmation of a viral aetiology came in 1971 when Padgett et al. isolated a virus from the brain of a patient who had died of PML. The patient's initials were J.C. The virus therefore became known as IC v i ru s . 7 JC virus is an ubiquitous infectious agent with JCspecific antibodies being detectable in approximately 65% of adolescents. 8 The virus persists for life in the kidney and may be shed in the urine of pregnant, elderly or immunosuppressed persons. 9' 10. ~, Little is understood of the mechanism whereby JC virus persists. More specifically, it is not known whether PML results from reactivation of JC virus and its spread from the kidney or if the virus initially establishes a latent CNS infection with subsequent reactivation in immunosuppressed persons. White and co-workers demonstrated the presence of ]C virus DNA in brain tissue from patients without PML. They suggested that persistent infection might be present in the absence of demyelinating disease. Prolonged immunosuppression or, alternatively, direct interaction with human immunodeficiency virus, might then activate the latent JC virus with subsequent development of PML. .2 Their observation favours the hypothesis that JC virus persists in both kidney and neurological tissue. Other workers, however, have found no evidence of JC virus persisting in brain tissue.13' 14 Clearly, understanding of the pathogenesis of this devastating disease is still incomplete. Progressive multifocal leukoencephalopathy results from a productive infection of oligodendrocytes, the myelin-forming cells, by JC virus. The infected cells undergo cytolytic destruction which results in loss of myelin so causing a relentlessly progressive and ultimately fatal neurological illness. This article will examine the clinical presentation, diagnosis and management of patients with PML.

A nested polymerase chain reaction-based method was used prospectively to detect herpesvirus DNA in cerebrospinal fluid (CSF) from 111 patients with AIDS, 39 of whom had a suspected diagnosis of cytomegalovirus (CMV)-associated neurologic disease (patients with encephalopathy, polyradiculopathy, or peripheral neuropathy) and 72 who had alternative diagnoses. CSF from 24 (62%) of the patients with suspected CMV-associated disease had detectable CMV DNA compared with only 8 (11%) of the patients with other diagnoses. Varicella-zoster virus DNA was detected in CSF from 3 patients (2 with myelitis and 1 with encephalitis), all of whom had recent cutaneous zoster. No CSF specimen contained detectable herpes simplex virus type 1 DNA, and none of the patients with myelitis had detectable herpes simplex virus type 2 DNA in CSF. This study demonstrates a significant association between detectable CMV DNA in CSF and suspected CMV-associated neurologic disease in patients with AIDS.

Kaposi sarcoma-associated herpesvirus (KSHV) is consistently found in biopsy samples from patients with AIDS-related and "classical" Kaposi's sarcoma (KS). Although highly suggestive of a causal role of KSHV in the pathogenesis of KS, this observation does not exclude the possibility that KSHV, like other herpesviruses, is widely distributed and is a mere "passenger" in these lesions. Here we report that KSHV was detectable in peripheral blood mononuclear cells of 24/46 (52%) of KS patients, but in none of 134 blood donors or 26 HIV-uninfected hospital controls. KSHV detection increased with immunosuppression, as shown by a correlation with a reduced number of CD4-positive T-cells. Moreover, KSHV detection in peripheral blood cells of HIV-infected individuals without KS predicted the subsequent appearance of KS lesions. 143 patients who did not have KS at the time of their first (or only) blood sample were followed up for a median of 30 months. Of the 11 who had been KSHV positive 6 developed KS compared with only 12 out of 132 who were KSHV negative. These findings are compatible with a causative role of KSHV in KS. KSHV was rarely detected in sputum and throat swabs of HIV-infected patients, providing a potential explanation for the apparently limited spread of this virus.

Over a 25-month period, six multiply transfused patients undergoing cytotoxic treatment for haematological or other malignant disorders developed icteric acute hepatitis B virus (HBV) infection. Bone marrow or peripheral-blood stem cells had been harvested from all six patients and stored in the same cryopreservation tank for possible future transplantation. Human DNA, HBsAg, and HBV DNA with sequences identical to those from four patients with related infections were subsequently found in the liquid nitrogen. Leakage of the cryopreservation bags used to store bone marrow harvested from the first patient when acutely infected with HBV led to contamination of the tank and its contents with HBV and subsequent transmission to patients after transplantation. This incident emphasises the continuing need to screen donors of tissue to be cryopreserved for bloodborne virus infections. It also reinforces the requirement for primary containers used to cryopreserve human tissue to be sealed in a way which prevents exchange of material between the specimen and the liquid nitrogen.

A cohort of 66 patients on maintenance haemodialysis was examined for serological (anti-HCV) and virological (HCV-RNA) evidence of infection with hepatitis C virus (HCV). Nine (13.6%) were anti-HCV positive, all of whom had detectable HCV-RNA in their serum. Statistical analysis of various risk factors (including length of time on haemodialysis, history of blood transfusion, history of renal transplantation and of previous hepatitis B infection) showed that only the length of time on haemodialysis was significantly associated with the acquisition of HCV infection. Genotypic analysis showed that five patients were infected with genotype 1 and a further two were infected with genotype 4. The latter finding is of significance because strains of genotype 4 are extremely uncommon in Western Europe. These results demonstrate that intra-unit transmission of HCV-infection took place in a group of patients on maintenance haemodialysis.

Acute meningoencephalitis and meningitis due to primary HIV infection {#article-title-2} A wide differential diagnosis exists for meningoencephalitis and meningitis: causes include tuberculosis and infections caused by viruses such as enteroviruses, human herpesviruses (types 1-4, 5 (cytomegalovirus), and 6), paramyxovirus (mumps), measles virus, and adenoviruses. In one cohort, viral genomes were detected in consecutive samples of cerebrospinal fluid from 5% of patients (22 of 410); enteroviruses and human herpesviruses types 1-5 accounted for over 95% of cases.1 HIV infection was not detected. It is often overlooked as a potential cause of meningoencephalitis and meningitis. The clinical manifestations of primary HIV infection are well characterised and include fever, lethargy, flu-like illness, headache, pharyngitis, generalised rash, lymphadenopathy, and gastrointestinal disturbances.2 Neurological features, including aseptic meningitis, meningoencephalitis, and encephalitis, occur in up to 17% of patients and may be associated with more rapid progression of HIV related disease.3–11 Neurological symptoms may occur or develop up to 3 months after the onset of symptoms of primary HIV infection, when the other symptoms have resolved. We discuss one patient with meningoencephalitis and two patients with meningitis associated with primary HIV infection. In each patient the underlying diagnosis of primary HIV infection was not suspected initially resulting in a delay to diagnosis. Over a 16 month period three men with viral symptoms had presented to their general practitioner (n=2) and local emergency department. One patient required immediate admission and the others were subsequently admitted through the emergency department and local genitourinary clinic. The patients failed to disclose any risk factor for acquiring HIV infection and none had clinical stigmata of immunosuppression. The table summarises the clinical details of these patients. Here we report on case 1. View this table: Clinical details of patients with primary HIV infection A 34 year old man presented with a one week history of fever, nausea, and confusion. The previous …

Summary. Patients undergoing therapy for haematological malignancies, who received blood products from United Kingdom (U.K.) donors who were unscreened for hepatitis C antibodies (anti-HCV), have previously been shown to be at risk of acquiring HCV (Brink et al., 1993). Screening for anti-HCV has recently been introduced into the U.K. and, in order to determine the efficacy of this in preventing transfusion-acquired HCV infection, we monitored a group of patients for possible acute HCV infection for 1 year after the introduction of donor screening in the U.K. We identified no new cases of HCV infection that were acquired in the U.K. during this period, thus demonstrating the efficacy of the currently available anti-HCV assays in preventing the majority of transfusion-acquired HCV infections.

Patients receiving multiple transfusions are at risk of acquiring hepatitis C (HCV) infection from a donor population which is unscreened for hepatitis C antibodies (anti-HCV). Prior to the introduction of blood donor screening for anti-HCV in the U.K., a group of patients undergoing therapy for haematological malignancies, with repeatedly abnormal liver function tests, were investigated for acute HCV infection. Thirty-two patients had repeatedly raised serum transaminases, and eight of these (25%) had evidence of an acute HCV infection. The diagnosis was made by the detection of HCV-RNA in the patients' serum using a complementary DNA/polymerase chain reaction (cDNA/PCR) procedure. All eight patients had received myeloablative chemotherapy and three had undergone bone marrow transplantation. HCV infection contributed significantly to the morbidity of this group of patients in the short term whilst they were undergoing treatment for their underlying haematological condition. The long-term effects have yet to be evaluated. In an attempt to decrease hepatic damage due to HCV, three patients were placed on interferon therapy. None showed a sustained reduction in serum transaminases or HCV viraemia. It is hoped that the introduction of anti-HCV screening of blood donors, will reduce the frequency of transfusion-acquired HCV infections. Early observations suggest that this is the case, as we have seen no new cases of HCV infection in our unit since the introduction of donor screening in September 1991.

This paper reports the failure of a patient suffering from Epidermodysplasia verruciformis, characterised by widespread infection of the skin with human papillomaviruses, to respond to topical and systemic treatment with the antiviral agent, Cidofovir, despite its previously demonstrated effectiveness against a range of different papillomavirus-associated conditions.

Summary Evidence suggests that nevirapine, a non-nucleoside reversetranscriptase inhibitor, might be very effective in the prevention of HIV-1 integration and the reduction of risk of HIV-1 acquisition after exposure. We used a triple combination regimen, including nevirapine, for prophylaxis after occupational or sexual exposure to HIV-1 infection. Of 57 individuals who started therapy, only 41 returned for follow-up. Five had a grade three or four drug-induced hepatitis, two of whom also had a rash. This high rate of major adverse events raises concerns over the safety of such a regimen for its use in this population.

Varicella zoster virus (VZV) is an uncommon but well recognized cause of neurological disease in HIV-infected patients. Analysis of cerebrospinal fluid (CSF) using the polymerase chain reaction (PCR) in HIV-infected patients presenting with neurological disease has increasingly allowed diagnosis of VZV-associated pathology. We report clinical, radiological and virological data from 15 consecutive patients with VZV-associated neurological disease. Clinical presentation was varied, including meningo-encephalitis in 9 and isolated cranial nerve palsies in 6. VZV deoxyribonucleic acid (DNA) was detected by PCR in CSF of 11/15; pleocytosis was present in only 6/15, raised protein in 11/15. Magnetic resonance imaging (MRI) appearances were focal signal abnormalities in 8, meningeal enhancement in 2 and normal in 2. With specific anti-VZV therapy 10 patients recovered fully. The predictive value of PCR on CSF for diagnosis of VZV-associated neurological disease should take into account the patient's clinical presentation, concurrent infections and response to anti-VZV therapy.

Objectives:To determine the frequency of detection of Kaposi’s sarcoma associated herpesvirus (KSHV), also known as human herpesvirus (HHV) type 8, DNA in bronchoalveolar lavage (BAL) fluid from HIV infected individuals with and without KS and to compare this with the detection rate in peripheral blood. Also to identify whether KSHV was associated with specific cell types in lavage fluid. Methods:Nested PCR was used to detect KSHV DNA in BAL fluid from 41 consecutive individuals with Kaposi’s sarcoma (KS) and in 41 controls with similar CD4 lymphocyte counts. Semiquantification of viral DNA was by end point titration. A positive cell sorting selection procedure was used to isolate specific BAL fluid cell types. Results: KSHV DNA was detected in BAL fluid from 24 of 29 (83%) individuals with a bronchoscopic diagnosis of tracheobronchial KS. None was detected in 12 individuals with only cutaneous KS, or in 41 matched controls without KS. In five, KSHV DNA was detected in the cell depleted and cellular fractions of BAL fluid and in 1/5 in the CD14 (macrophage) fractions. None was detected in the CD19 (B lymphocyte) or CD4/CD8 (T lymphocyte) fractions. Conclusions: There was a clear association between the diagnosis of tracheobronchial KS and detection of KSHV DNA in BALfluid. The cell type supporting KSHV in the respiratory tract is not CD 19 positive and has yet to be conclusively identified. (Sex Transm Inf 1998;74:27‐31)

A total of 95 patients who presented in 1994 and 1995 with focal brain lesions at a London HIV centre were studied retrospectively. Patients were allocated to "definite" or "presumed" diagnostic categories of toxoplasma encephalitis (TE), primary CNS lymphoma (PCNSL) or progressive multifocal leukoencephalopathy (PML), based on strict criteria. The number in each category was: TE, 20; PCNSL, 9; PML, 7; presumed TE, 12; presumed PCNSL, 8 and presumed PML, 17. There were 20 patients in whom a diagnosis could not be made, and there were three non-HIV diagnoses. Demographic data, features at presentation and routine CSF analysis were not discriminatory in making a diagnosis. Toxoplasma titres were a median of 1:256 in those with TE compared to 1:16 in all other groups (p < 0.001) and those with TE were less likely to be on toxoplasma prophylaxis compared to those with PCNSL (p < 0.002). Survival with TE (median of 446 days) was significantly longer than survival in all other groups. Survival with either confirmed or presumed PML was similar. The problems of diagnosis of focal brain lesions in HIV patients are discussed and a management flow chart for mass lesions is proposed.

A 14-year-old girl with HIV infection and subcutaneous Kaposi's sarcoma (KS) received thalidomide therapy for oral ulcers, resulting in regression of KS lesions, disappearance of KS-associated herpesvirus (KSHV) DNA from blood, and reduced viral load in tumor tissue. Administration of granulocyte colony-stimulating factor resulted in clinical exacerbation of KS and reappearance of KSHV DNA in blood.

OBJECTIVES: To evaluate the contribution of community-based respiratory virus infections to lower respiratory tract disease in HIV-1 infected individuals. DESIGN: Prospective clinical cohort study. SETTING: Specialist in-patient unit for HIV and AIDS, University College London Hospitals, London. SUBJECTS: 44 consecutive HIV-1 antibody positive patients who underwent 47 diagnostic bronchoscopies for evaluation of the symptoms and signs of lower respiratory tract disease. TIME: Winter months of 1994/95. MAIN OUTCOME MEASURES: Detection, in bronchoscopic alveolar lavage fluid, of infection with influenza A and B, respiratory syncytial virus (RSV), parainfluenza 1, 2 and 3 (by immunofluorescence and cell culture) and adenovirus and enteroviruses (by cell culture). RESULTS: No evidence of influenza, RSV, parainfluenza, adenovirus, or enterovirus infection was detected. CONCLUSIONS: Despite a marked increase in RSV and influenza B infection in the general population over the winter of 1994-95, respiratory virus infections were not detected in this cohort of HIV infected patients. As the organisms causing lower respiratory tract disease were related to immunosuppression, this study questions the value of routine identification of community-based respiratory viruses in this patient group.

A Caucasian homosexual man with AIDS and cytomegalovirus retinitis presented with facial pain and episodic confusion, had several seizures and became obtunded. An electroencephalogram was suggestive of herpes simplex encephalitis. The diagnosis was confirmed by detection of herpes simplex virus type 2 (HSV 2), but not type 1, DNA in cell-free cerebrospinal fluid (CSF) after amplification by nested polymerase chain reaction. The patient also had evidence of concomitant cytomegalovirus (CMV) infection with detectable CMV DNA in CSF. With high-dose acyclovir the patient recovered. Analysis of a follow up CSF sample taken four months later showed no detectable HSV-2 DNA.