Short-term steroid treatment of Rhesus macaque increases transduction

2021 ◽  
Author(s):  
Murali K Yanda ◽  
Vartika Tomar ◽  
Cristina Cebotaru ◽  
William Guggino ◽  
Liudmila Cebotaru
1973 ◽  
Vol 13 (1-2) ◽  
pp. 100-114 ◽  
Author(s):  
S.R. Ojeda ◽  
V.D. Ramirez
Keyword(s):  

1984 ◽  
Vol 61 (5) ◽  
pp. 983-985 ◽  
Author(s):  
Avital Fast ◽  
Malvina Alon ◽  
Shmuel Weiss ◽  
Freddy R. Zer-Aviv

✓ The authors present a case of avascular necrosis of both femoral and humeral heads which developed after short-term steroid treatment for brain edema. Avascular necrosis of bone may develop after short-term as well as after maintenance steroid therapy. Early diagnosis with bone scanning and management may in some cases prevent joint destruction.


1995 ◽  
Vol 29 (12) ◽  
pp. 1235-1237 ◽  
Author(s):  
Dolors Conesa ◽  
Jordi Rello ◽  
Jordi Vallés ◽  
Dolors Mariscal ◽  
Joan Carles Ferreres

Objective: To describe a patient with invasive pulmonary aspergillosis related to short-term steroid treatment. Case Summary: A 78-year-old man with chronic obstructive pulmonary disease (COPD) developed an invasive pulmonary aspergillosis after short-term (less than 1 week) intravenous steroid therapy. The diagnosis was established by recovering Aspergillus fumigatus from a bronchoalveolar lavage and was confirmed by autopsy, with the additional finding of an aspergilloma. Discussion: This case is of interest for 3 reasons: (1) it illustrates that invasive aspergillosis may be followed by a rapidly progressive respiratory failure, even in the absence of a fever; (2) this patient had simultaneously an aspergilloma and an invasive aspergillosis; and (3) it confirms reports indicating that short-term steroid therapy for COPD represents a significant risk factor for opportunistic lung infections. Conclusions: In patients with COPD who receive even short-term steroid therapy and who have progressive respiratory failure caused by pneumonia, invasive aspergillosis should be suspected early and acted upon accordingly.


2021 ◽  
Vol 7 (2) ◽  
pp. 134-136
Author(s):  
Fatma Şimşek

Orbital myositis is an inflammatory disease affecting extraocular muscles. Mostly unilateral and rarely bilateral orbital involvement is seen. Bilateral involvement is a secondary table to systemic diseases and recurrence can be seen. Diagnosis is made by clinical, examination and imaging. Increased density of extraocular muscles and increased muscle mass should be seen in computed tomography or magnetic resonance imaging. The basis of the diagnosis is exclusion and the differential diagnosis needs to be done well. Steroids and other immunosuppressive agents may be used in the treatment. Patients respond dramatically to steroid treatment. While short-term steroid treatment may be sufficient in idiopathic patients, orbital myositis secondary to systemic disease requires longer-term and non-steroid immunosuppressive treatments. Here, a case of idiopathic orbital myositis with bilateral involvement is presented as it is a rare condition.


2019 ◽  
Author(s):  
Ria Goswami ◽  
Ashley N. Nelson ◽  
Joshua J. Tu ◽  
Maria Dennis ◽  
Liqi Feng ◽  
...  

ABSTRACTTo achieve long-term viral remission in HIV-infected children, novel strategies beyond early anti-retroviral therapy (ART) will be necessary. Identifying clinical predictors of time to viral rebound upon ART interruption will streamline the development of novel therapeutic strategies and accelerate their evaluation in clinical trials. However, identification of these biomarkers is logistically challenging in infants, due to sampling limitations and potential risks of treatment interruption. To facilitate identification of biomarkers predicting viral rebound, we have developed an infant rhesus macaque (RM) model of oral SHIV.CH505.375H.dCT challenge and analytical treatment interruption (ATI) after short-term ART. We used this model to characterize SHIV replication kinetics and virus-specific immune responses during short-term ART or post-ATI and demonstrated plasma viral rebound in 5 out of 6 (83%) infants. We observed a decline in humoral immune responses and partial dampening of systemic immune activation upon initiation of ART in these infants. Furthermore, we documented that infant and adult macaques have similar SHIV replication and rebound kinetics and equally potent virus-specific humoral immune responses. Finally, we validated our models by confirming a well-established correlate of time to viral rebound, namely pre-ART plasma viral load, as well as identified additional potential humoral immune correlates. Thus, this model of infant ART and viral rebound can be used and further optimized to define biomarkers of viral rebound following long-term ART as well as to pre-clinically assess novel therapies to achieve a pediatric HIV functional cure.IMPORTANCENovel interventions that do not rely on daily adherence to ART are needed to achieve sustained viral remission for perinatally infected children who currently rely on lifelong ART. Considering the risks and expense associated with ART-interruption trials, identification of biomarkers of viral rebound will prioritize promising therapeutic intervention strategies, including anti-HIV Env protein therapeutics. However, comprehensive studies to identify those biomarkers are logistically challenging in human infants, demanding the need for relevant non-human primate models of HIV rebound. In this study, we developed an infant RM model of oral Simian/Human Immunodeficiency virus infection expressing clade C HIV Env, and short-term ART followed by ATI, longitudinally characterizing immune responses to viral infection during ART and post-ATI. Additionally, we compared this infant RM model to an analogous adult RM rebound model and identified virologic and immunologic correlates of time to viral rebound post-ATI.


2014 ◽  
Vol 14 (12) ◽  
pp. 2954-2958 ◽  
Author(s):  
Kyung-Jin Song ◽  
Su-Kyung Lee ◽  
Jong-Hyun Ko ◽  
Myung-Jae Yoo ◽  
Do-Yeon Kim ◽  
...  

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4652-4652
Author(s):  
Ming Hung Hu ◽  
Chun-Yu Liu ◽  
Cheng-Hwai Tzeng

Abstract Abstract 4652 Patient with refractory ITP have increased mortality compared with the normal population. Apart from major bleeding, infection was a major risk of death of these patients.1However, infections after diagnosis of immune thrombocytopenia are less addressed in the literature and its clinical impact on outcome of patients with ITP has not been well-addressed. This study aimed to characterize risk of infection events after diagnosis of ITP and its impact on outcome of these patients. We retrospectively evaluated 239 patients (109 men, 130 women; medium age: 63 yr) diagnosed between Jan 1, 1997 to Aug 31, 2011. Every patient received at least steroid treatment according to platelet count or bleeding symptoms after diagnosis. Infection event occurred in 59 patients (24.7%) within 6 months after diagnosis. Multivariate analysis revealed that age (>65 yr) was the most important risk factor regarding to infection (p=0.048, 95% CI 1.005 to 4.007). 1-year mortality rate after ITP diagnosis was significantly higher in those patients with infection after steroid treatment (p<0.001). We conclude that elderly patients with ITP are more prone to infections which have negative impact on post-diagnosis 1 year survival. Table 1. The Demographic and Clinical Characteristics of Patients With Immune Thrombocytopenia Patient characteristic All patients (n=239) Sex, no. of patients (%) Male 109 (45.6%) Female 130 (54.4%) Medium age, y 63.0 (18∼97) Medium follow-up period, months 19.08 (0.1∼155) Thrombocytopenia1 no. of patients (%) 195 (81.6%) Severe 44 (18.4%) Moderate 20 (8.4%) Evan's syndrome, no. of patients (%) 19 (7.9%) Splenectomy, no. of patients (%) 35 (14.6%) Comorbidity, no. of patients (%) 74 (31%) DM 12 (5%) HTN 8 (3.3%) CKD 12 (5%) CHF 8 (3.3%) CVA 96 (40.2%) COPD 59 (24.7%) Any 13 (5.4%) Infectious event, no. of patients (%) 11 (4.6%) Total patient 2 (0.8%) Mortality, no. of patients (%) Total numbers Death due to infection Death due to bleeding 1. Moderate thrombocytopenia= platelet counts between 30.0 × 109/L and 100.0 × 109/L; severe thrombocytopenia counts below 30.0 × 109/L. Table 2. Clinical Characteristics of Infection Events Patient characteristic All events (n=70) Infectious event, no. (%) Total event 70 Pneumonia 31 (44.2%) UTI 13 (15.6%) Herpes zoster 9 (12.8%) Cellulitis 7 (10.0%) Others1 10 (14.3%) Pathogens no. of event Events with definite cultured pathogen 29 Staphylococcus aureus 8 Klebsiella pneumonia 6 Yeast2 6 Pseudomonas aeruginosa 5 Acinetobacter baumannii 4 Stenotrophomonas maltophilia 4 E. coli 3 Enterobacter spp. 3 Others3 5 Infection event date 1st month 23 (32.9%) 2nd month 17 (24.3%) 3rd month 7 (10.0%) 4th month 8 (11.4%) 5th month 6 (8.5%) 6th month 9 (12.9%) 1. Other infection includes oral candidiasis (2), cholangitis (1), fungemia (1), bacteremia (1), intraabdominal abscess (1), facial abscess (1), osteomyelitis (1), pseudomembranous colitis (1), acute suppprative periodontitis (1). 2. Including Candida albicans and Aspergillus. 3. Other pathogen including Streptococcus agalactiae (1), Serratia spp (1) Clostridium dificile (1), Chryseobacterium meningosepticum (1), gram positive cocci (1). Table 3. Baseline Characteristics of Patients with or without Infection Character No infection (n=180) Infection (n=59) p value Sex 0.006* M 73 (40.6%) 36 (61.0%) F 107 (59.4%) 23 (39.0%) Age 0.616 Medium 57 73 Range 18∼90 23∼97 Thrombocytopenia 0.268 Moderate 36 (20.0%) 8 (13.6%) Severe 144 (80.0%) 51 (86.4%) Evan's syndrome 14 (7.8%) 6 (10.2%) 0.565 Splenectomy 13 (7.2%) 6 (10.2%) 0.468 Cormobidity DM 21 (11.7%) 14 (23.7%) 0.023* HTN 51 (28.3%) 23 (39.0%) 0.125 CKD 6 (3.3%) 6 (10.2%) 0.037* CHF 5 (2.8%) 3 (5.1%) 0.393 CVA 8 (4.4%) 4 (6.8%) 0.476 COPD 4 (2.2%) 4 (6.8%) 0.095 Any 64 (35.8%) 31 (52.5%) 0.022* ANC<1000 49 (27.2%) 26 (44.1%) 0.016* Response1 0.001* CR+PR 151 (83.9%) 38 (64.4%) NR 29 (16.1%) 21 (35.6%) 1. Response: complete response (CR) partial response (PR) no response (NR). Table 4. Multivariate Analysis for the Short Term (Within 6 Months) Infection Risk in Patient with ITP Dependant variable Odds ratio P value 95% confidence interval Lower bound Upper bound Age >65 2.205 0.048* 1.005 4.077 ALC<1000 1.807 0.066 0.961 3.399 Any cormobidity 1.374 0.357 0.699 2.699 Disclosures: No relevant conflicts of interest to declare.


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