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Virion concentration in bronchoalveolar lavage fluids of HIV Infected patients
Letters to the Editor
Virion concentration in bronchoalveolar lavage fluids of HIV Infected patients SiR-Health-care workers exposed to bronchoalveolar lavage (BAL) fluids from HIV infected patients could be at risk of infection. Although lung cells from seropositive subjects are potential sources of infectious HIV/ whether these cells are productively or latently infected by the virus in vivo is unknown. We have measured free virions in the concentrated cell-free BAL fluid of HIV-infected subjects. 25 HIV-seropositive subjects underwent BAL. RNA was extracted from the virus pellet of 50 mL BAL fluid. HIV genomic RNA was detected by reverse transcription polymerase chain reaction (PCR)2 in the BAL acellular fluids of all subjects. The number of free HIV virions was:
Mean
(SE, range).
’PCP
vs no
pulmonary infection--CDC stage: IVC1 vs IVA-IVD; CD4
Because of the dilution of epithelial
lining fluid induced by by calculating the number of
BAL, we standardised our data free viral particles per gram of albumin in the BAL fluid. An almost 10 fold increase in virion number was found in the subjects with Pneumocystis carinii pneumonia (PCP) compared with those without pulmonary infection (p=0001,t test). Although the albumin correction factor tends to be higher in the PCP group (mean 37 fold increase) than in the non-PCP group (mean 15 fold increase), this was not statistically
significant. Our detection of HIV virions in cell-free BAL fluid of all patients shows the virus replicates in the lower respiratory tract of patients with symptomatic HIV infection. Compared with the concentration of HIV virions in the peripheral blood of patients with advanced disease,3 the virion number in BAL varied considerably according to whether or not there was PCP. This finding agrees with our work demonstrating a higher frequency of infectious HIV-harbouring lung cells in patients with PCP compared with subjects without pulmonary infection.4 The increased virion numbers in the BAL of patients with PCP might be related to a local activation of immune/ inflammatory responses, as occurs in peripheral blood.5 Some of the mediators involved in such responses are known to upregulate viral replication in vitro and are released in PCP.6 Although HIV core p24 antigen (a marker for viral replication) could not be detected in BAL fluids by enzyme-linked immunoassay,7 our reverse transcription PCR demonstrated the presence of HIV virions in all the BAL fluids of 25 AIDS and AIDS-related-complex patients. The virion concentration could be enhanced by active opportunistic pulmonary infections, such as PCP. BAL fluids of patients with symptomatic HIV infection may be contagious. Wei Lu,
Dominique Israël-Biet
298
1498-99. Lu W, Shih WKJ, Andrieu JM. Quantitation of HIV-1 RNA viremia and infectious virus-carrying cell frequency in the blood of HIV-1 infected symptom-free individuals. VIII International Conference on AIDS/III STD World Congress. Harvard-Amsterdam Conference, 1992: abstr PoA 2117. 4 Israël-Biet D, Cadranel J, Even P. HIV production by alveolar lymphocytes is increased during Pneumocystis carinii pneumonial Am Rev Respir Dis (in press). 5 Ho DD. HIV-1 viraemia and influenza. Lancet 1992; 339: 1549. 6 Israël-Biet D, Cadranel J, Beldjord K, Andrieu JM, Jeffrey A, Even P. Tumor necrosis factor production in HIV-seropositive subjects: relationship with lung opportunistic infections and HIV expression in alveolar macrophages. J Immunol 1991; 147: 490-04. 7 Rose RM, Krivine AM, Pinkston P, Gillis JM, Huang A, Hammer SM. Frequent identification of HIV-DNA in bronchoalveolar lavage cells obtained from individuals with the acquired immunodeficiency syndrome. Am Rev Respir Dis 1991; 143: 850-04. 3
count
j (/ftL): 40-148 (n= 7) vs 15-422 (n= 10)..
Laboratorie d’immunologie des Tumeurs, Hôpital Laënnec, Université de Paris V, 75007 Paris. France
Jeffrey AA, Israël-Biet D, Andrieu JM, Even P, Venet A. HIV isolation from pulmonary cells derived from bronchoalveolar lavage. Clin Exp Immunol 1991; 85: 488-92. 2 Lu W, Andrieu JM. Use of the human immunodeficiency virus virion as a universal standard for viral RNA quantitation by reverse transcription-linked polymerase chain reaction. J Infect Dis 1993; 167: 1
Trichinella pseudospiralis In
man
SiR-Trichinella pseudospiralisl has been reported as a potential human pathogen.2 We describe a case that points to a disease entity distinct from classic trichinosis. Several of the features of this case had been earlier predicted in experimental infections of monkeys with T pseudospiralis.3 The patient is a 33-year-old woman who for at least 5 years had had tiredness, muscle fatigue, and muscle pain after exercise. Blood tests showed raised transaminases and mild eosinophilia, which later resolved. Creatine kinase fluctuated at high levels (3294-5532 IU/L). Electromyography suggested myositis and deltoid muscle biopsy showed polymyositis. Review of the biopsy slides after weakness developed during steroid treatment for myositis led to a further biopsy and the discovery of mobile unencapsulated larvae identified as T pseudospiralis. Symptoms that appeared at various times until treatment for trichinella included racing heart and palpitations, fatigue, muscle pain, swallowing difficulties, and periorbital oedema. Frequent travel by the patient, changes of doctor, and general protean symptoms delayed firm diagnosis. Immunosuppressive therapy for myositis worsened her condition. Diagnosis of pseudospiralis trichinosis was followed by treatment with albendazole4 which, initially accompanied by prednisone, brought quick results, with creatine kinase returning to normal within 3 weeks and a loss of most symptoms. Some ache was reported in the leg muscles for 4 months. Among the unusual features was the length of time the larvae were.presumed active in the muscle of the patient(around 7 or more years). The source of the infection was difficult to pinpoint, but as the patient had spent some time in Tasmania, where T pseudospiralis has been previously recorded,s it was assumed that she acquired the infection there rather than in New Zealand, where it was eventually detected. Infected wallaby meat or pork were considered as possible sources.
Virion concentration in bronchoalveolar lavage fluids of HIV Infected patients SiR-Health-care workers exposed to bronchoalveolar lavage (BAL) fluids from HIV infected patients could be at risk of infection. Although lung cells from seropositive subjects are potential sources of infectious HIV/ whether these cells are productively or latently infected by the virus in vivo is unknown. We have measured free virions in the concentrated cell-free BAL fluid of HIV-infected subjects. 25 HIV-seropositive subjects underwent BAL. RNA was extracted from the virus pellet of 50 mL BAL fluid. HIV genomic RNA was detected by reverse transcription polymerase chain reaction (PCR)2 in the BAL acellular fluids of all subjects. The number of free HIV virions was:
Mean
(SE, range).
’PCP
vs no
pulmonary infection--CDC stage: IVC1 vs IVA-IVD; CD4
Because of the dilution of epithelial
lining fluid induced by by calculating the number of
BAL, we standardised our data free viral particles per gram of albumin in the BAL fluid. An almost 10 fold increase in virion number was found in the subjects with Pneumocystis carinii pneumonia (PCP) compared with those without pulmonary infection (p=0001,t test). Although the albumin correction factor tends to be higher in the PCP group (mean 37 fold increase) than in the non-PCP group (mean 15 fold increase), this was not statistically
significant. Our detection of HIV virions in cell-free BAL fluid of all patients shows the virus replicates in the lower respiratory tract of patients with symptomatic HIV infection. Compared with the concentration of HIV virions in the peripheral blood of patients with advanced disease,3 the virion number in BAL varied considerably according to whether or not there was PCP. This finding agrees with our work demonstrating a higher frequency of infectious HIV-harbouring lung cells in patients with PCP compared with subjects without pulmonary infection.4 The increased virion numbers in the BAL of patients with PCP might be related to a local activation of immune/ inflammatory responses, as occurs in peripheral blood.5 Some of the mediators involved in such responses are known to upregulate viral replication in vitro and are released in PCP.6 Although HIV core p24 antigen (a marker for viral replication) could not be detected in BAL fluids by enzyme-linked immunoassay,7 our reverse transcription PCR demonstrated the presence of HIV virions in all the BAL fluids of 25 AIDS and AIDS-related-complex patients. The virion concentration could be enhanced by active opportunistic pulmonary infections, such as PCP. BAL fluids of patients with symptomatic HIV infection may be contagious. Wei Lu,
Dominique Israël-Biet
298
1498-99. Lu W, Shih WKJ, Andrieu JM. Quantitation of HIV-1 RNA viremia and infectious virus-carrying cell frequency in the blood of HIV-1 infected symptom-free individuals. VIII International Conference on AIDS/III STD World Congress. Harvard-Amsterdam Conference, 1992: abstr PoA 2117. 4 Israël-Biet D, Cadranel J, Even P. HIV production by alveolar lymphocytes is increased during Pneumocystis carinii pneumonial Am Rev Respir Dis (in press). 5 Ho DD. HIV-1 viraemia and influenza. Lancet 1992; 339: 1549. 6 Israël-Biet D, Cadranel J, Beldjord K, Andrieu JM, Jeffrey A, Even P. Tumor necrosis factor production in HIV-seropositive subjects: relationship with lung opportunistic infections and HIV expression in alveolar macrophages. J Immunol 1991; 147: 490-04. 7 Rose RM, Krivine AM, Pinkston P, Gillis JM, Huang A, Hammer SM. Frequent identification of HIV-DNA in bronchoalveolar lavage cells obtained from individuals with the acquired immunodeficiency syndrome. Am Rev Respir Dis 1991; 143: 850-04. 3
count
j (/ftL): 40-148 (n= 7) vs 15-422 (n= 10)..
Laboratorie d’immunologie des Tumeurs, Hôpital Laënnec, Université de Paris V, 75007 Paris. France
Jeffrey AA, Israël-Biet D, Andrieu JM, Even P, Venet A. HIV isolation from pulmonary cells derived from bronchoalveolar lavage. Clin Exp Immunol 1991; 85: 488-92. 2 Lu W, Andrieu JM. Use of the human immunodeficiency virus virion as a universal standard for viral RNA quantitation by reverse transcription-linked polymerase chain reaction. J Infect Dis 1993; 167: 1
Trichinella pseudospiralis In
man
SiR-Trichinella pseudospiralisl has been reported as a potential human pathogen.2 We describe a case that points to a disease entity distinct from classic trichinosis. Several of the features of this case had been earlier predicted in experimental infections of monkeys with T pseudospiralis.3 The patient is a 33-year-old woman who for at least 5 years had had tiredness, muscle fatigue, and muscle pain after exercise. Blood tests showed raised transaminases and mild eosinophilia, which later resolved. Creatine kinase fluctuated at high levels (3294-5532 IU/L). Electromyography suggested myositis and deltoid muscle biopsy showed polymyositis. Review of the biopsy slides after weakness developed during steroid treatment for myositis led to a further biopsy and the discovery of mobile unencapsulated larvae identified as T pseudospiralis. Symptoms that appeared at various times until treatment for trichinella included racing heart and palpitations, fatigue, muscle pain, swallowing difficulties, and periorbital oedema. Frequent travel by the patient, changes of doctor, and general protean symptoms delayed firm diagnosis. Immunosuppressive therapy for myositis worsened her condition. Diagnosis of pseudospiralis trichinosis was followed by treatment with albendazole4 which, initially accompanied by prednisone, brought quick results, with creatine kinase returning to normal within 3 weeks and a loss of most symptoms. Some ache was reported in the leg muscles for 4 months. Among the unusual features was the length of time the larvae were.presumed active in the muscle of the patient(around 7 or more years). The source of the infection was difficult to pinpoint, but as the patient had spent some time in Tasmania, where T pseudospiralis has been previously recorded,s it was assumed that she acquired the infection there rather than in New Zealand, where it was eventually detected. Infected wallaby meat or pork were considered as possible sources.